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First Fern Genome Shows Unique Bacterial Partnership - D-brief - Discover

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Bacteria in the ferns' leaves help them acquire nitrogen from the air, a partnership researchers probe with genetic sequencing.

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First Fern Genome Shows Unique Bacterial Partnership - D-brief - Discover

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Pollution killing fungi vital for plant growth

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Pollution killing fungi vital for plant growth

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Scientists are warning that pollution could be starving Europe's trees of vital nutrients by damaging essential fungi.

The fungi live on the roots of trees, supplying them with minerals and water.

Current pollution limits may not be strict enough to protect the forest fungi, say researchers.

Signs of tree malnutrition, such as discoloured or missing leaves, have been seen across Europe's forests.

Loss of fungi may be a factor, according to the study, published in the journal, Nature.

"If we care about the condition of our forests - what shape they're in - we can't just look above (the ground)," Dr Martin Bidartond, from the department of life sciences at Imperial College London and Royal Botanic Gardens, Kew, told BBC News.

"We need to look below - we need to understand how the fungi are nourishing the trees."

Double life

Fungi can be found living on the roots of trees, providing vital nutrients and water.

Known by the truffles and mushrooms formed by some species, they can live for decades beneath the surface, growing to several square metres in size.

These fungi, known as mycorrhizal fungi, receive carbon from the tree in exchange for essential nutrients, like nitrogen, phosphorous and potassium, which they take up from the soil.

The researchers studied 40,000 roots from 13,000 soil samples at 137 forest sites in 20 European countries, including the UK, over 10 years.

They found local air and soil quality have a large impact on mycorrhizae.

"Trees need this fungi to get nutrients and water from soil and there are factors like pollution that are affecting this fungi," said Dr Laura M Suz of the Royal Botanic Gardens, Kew, a co-researcher on the study.

"We need to be aware of it at least because these fungi are essential for the growth and the health of the trees."

The researchers say these first large-scale results should be used to design new studies into the link between pollution, soil, mycorrhizae, tree growth and tree health.

"A major finding of the study is that European pollution limits may be set far too high," said Dr Bidartond.

"In North America the limits are set much lower, and we now have good evidence they should be similar in Europe. For example, current European nitrogen limits may need to be cut by half. Our trees in Europe are not more tolerant than those in North America - their fungi are just suffering more."

The study looked at beech, oak, pine and spruce trees across Europe, including several oak, pine and beech forests in the UK.

Fungi receive little protection under conservation policies, which makes it hard to assess which species are rare or declining.

Follow Helen on Twitter.

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Scientists are warning that pollution could be starving Europe's trees of vital nutrients by damaging essential fungi. The fungi live on the roots of trees, supplying them with minerals and water. Current pollution limits may not be strict enough to protect the forest fungi, say researchers.

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The race to sequence the human genome - Tien Nguyen

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0:00 / 39:25•Watch full video

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Astronaut Scott Kelly's DNA didn't mutate in space....epigenetics

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Astronaut Scott Kelly's DNA didn't mutate in space....epigenetics

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If you believe recent news, NASA astronaut Scott Kelly went to space, spent a year there, and came back with substantial changes to his DNA. Some outlets are even reporting that a whopping seven percent of Kelly's genes-segments of DNA that code for various proteins-are "abnormal" post-spaceflight.

Unfortunately, even Kelly appears to be surprised by the news.

"What? My DNA changed by 7%! Who knew? I just learned about it in this article. This could be good news! I no longer have to call [Mark Kelly] my identical twin brother anymore," Scott Kelly tweeted.

Well, and we hate to spoil the fun, but no. The story Kelly is referring to, and many more, misrepresent the results of a study NASA commissioned on the effects of spaceflight by confusing changes in genetic sequence with changes in gene expression levels.

That study, which involves multiple independent research groups, compared Scott with his twin brother Mark (also a NASA astronaut) and looked for changes caused while Scott spent a year aboard the International Space Station, a mission that ended in March 2016. Among the dimensions surveyed were cognitive ability, immune system function, and genetics.

The space agency says that papers detailing the findings will be published later this year, and for now, the press is mostly relying on some vague wording and other information contained in a NASA release.

"I, too, am concerned about how the stories coming out are being sensationalized," says Colorado State University's Susan Bailey, who leads one of the research groups studying the twins.

So, no, seven percent of Kelly's DNA is not mutated after his year in space, which makes sense if you keep in mind that humans and chimps have genetic sequences that differ by less than 2 percent, and individual humans-even completely unrelated strangers-differ by about 0.1 percent.

Here's how this works.

Genetic sequences are like strings of letters arranged just so, and they are in charge of producing proteins. Mutate the wrong letter, or sequence of letters, and it can be mildly annoying, like our favorite ducking autocorrect, or it can be extremely bad news, like the mutations that allow tumors to proliferate. Most mutations, however, go unnoticed (the one that confer superpowers are a different story).

Expression levels, on the other hand, reflect whether genes are turned on or turned off. Within each of us, most of our cells are otherwise genetically identical, but their genes are expressed at different levels. It's those patterns of expression that produce hearts, brains, eyeballs, and other things, kind of like using the same set of ingredients to cook up vastly different dishes.

The NASA result everyone is freaking out about actually measured Scott Kelly's expression levels, and it found that-not surprisingly-spaceflight affects how much expressing certain genes do, particularly those involved in immune function, DNA repair pathways, and bone growth.

"Seven percent of the genes that changed their expression during spaceflight were still altered after six months back on Earth," says Weill Cornell Medicine's Christopher Mason, who led the analysis.

That these levels of expression haven't boomeranged to pre-spaceflight values is humongously different than saying Kelly's DNA didn't " return to normal after a sojourn in space."

"We had no idea what to expect, and this is the first experiment of its kind, so this sets the bar for future studies of astronauts," Mason says. "Nonetheless, this number is likely within the range for humans under stress, such as climbing a mountain, or SCUBA diving."

Indeed, seeing such changes in expression is not at all unusual-it happens each time we get sick, or in response to environmental factors. Certainly, spending a year in microgravity with reduced oxygen and increased radiation levels could cause that type of change.

Mark and Scott Are Not Identical

Another somewhat alarming-sounding finding is that Scott Kelly's DNA " no longer matches that of his identical twin."

For anyone familiar with genetics, this is possibly the most obvious statement one could make. We humans accumulate random mutations throughout our genomes as we age, and the chances that Mark and Scott's genetic sequences were randomly modified in exactly the same way are astronomically small. In reality, their DNA hasn't been identical for most of their lives.

That's just at the most basic sequence level. All sorts of chemical modifications to DNA can dramatically affect where and how genes are expressed, and those markings-termed epigenetic-are malleable. Genomes add and erase those markings all the time, and they're not the same between identical twins, either.

Throw in a heaping pile of spaceflight, where exposure to higher levels of radiation necessarily mutates DNA more quickly, and the truly surprising result would be seeing no difference between Mark's and Scott's genetic sequences. The fact that they differ, and that Scott's mutation rate is apparently a bit higher than Mark's, is totally expected.

"No twin pairs are ever completely identical, and we all do accrue random mutations all the time," Bailey says. "No doubt, Scott did or does have different or more mutations than Mark-and anyone else not being in space for a year-due to radiation exposure alone."

Chromosomal Bungee Cords

All of that being said, one of the actually surprising findings from the NASA study is that Kelly's chromosomes grew longer while he was in space, at least in his white blood cells. The changes occurred in what's known as the telomere, a cap of genetic material that sits at the end of each chromosome.

Normally, telomeres shrink with age, the idea being that each time a chromosome is copied during cell division, the process chips away at that cap. Shortened or frayed telomeres are largely thought to be responsible for age-related cellular breakdown.

But Kelly's telomeres elongated in space ... and then quickly shrank to their original lengths after he returned to Earth. That these structures exhibit such flexibility is intriguing and potentially quite consequential, says Bailey, whose lab studied Kelly's telomeres.

"We're now trying to figure out why and what caused such shifts, so we can better appreciate potential health risks," Bailey says, though she also notes that Scott Kelly's exercise and nutrition on the station likely contributed to the chromosomal bungee.

All this means that if Scott really wanted to no longer be genetically identical to Mark, he didn't need to spend a year in space.

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No, Scott Kelly's Year in Space Didn't Mutate His DNA

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If you believe recent news, NASA astronaut Scott Kelly went to space, spent a year there, and came back with substantial changes to his DNA. Some outlets are even reporting that a whopping seven percent of Kelly's genes-segments of DNA that code for various proteins-are "abnormal" post-spaceflight.

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Having five senses at our disposal seems great, until you realise many animals have either bettered these senses or created entirely new ways of experiencing the world around them. Here are some of the special animal senses evolved over millions of years, that give them the edge over our human senses.

Vision

Our eyesight as a species is by no means poor: unlike many others, we can see in colour using three types of colour detecting receptors called cone cells. Each type of cone cell detects a different colour, which amalgamate to give us the rainbow of colours which paint our surroundings.

But that doesn't mean ours is the best sense of sight. Our measly three cone cell types are trumped by a tiny creature sporting an incredible 15 different types of cone cell: the humble shrimp. Look around at all the colours you can see and try to imagine seeing five times as many - it's mind-boggling!

While the visual spectrum for humans stretches from purple to red with the rest of the rainbow slotting in between, some animals have extended their visual spectrum into the ultraviolet and the infrared...
Ultraviolet
Bees can process ultraviolet light (the same light we block out with sun cream) to make the flowers they target more vivid and ensure the pollen stands out.
Caribou Spot Wolves Using UV Vision | Animal Super Senses | BBC (YouTube/BBC Earth)
This is impressive but more amazing still is that reindeer can change their perception of light dependent on the season. Santa's helpers adapt to the scarcity of food in the winter months by stretching their visual field into the ultraviolet so that the lichen they feed on glows a striking purple against the white blanket of snow. It also helps avoid falling prey to wolves, whose coats don't reflect UV, making them appear black against the snow in the reindeer's eyes.
Infrared
Infrared equipment like goggles and cameras help humans see in the dark by converting the heat of the surrounding environment into a coded image with the coldest areas shown in black and the hottest in white.

Certain species of snake can do this without needing specialist equipment; they simply have holes below their eyes called pit organs which house receptors that can detect heat emitted up to a metre away. This heat is mapped over the snake's visual representation of its surroundings to create a multi-dimensional image allowing it to pin-point prey in all light levels.
Night-vision
Light of some sort is compulsory for vision. How, then, can some animals see in the dark? You may have noticed that nocturnal animals' eyes shine bright in the darkness - this isn't a trick of the light. It's actually one of their secret adaptations for night-vision.

They reflect light back out of their eyes thus giving the light-sensitive cells in the retina of their eyes two chances to catch as many particles of light as possible which makes the world around them appear brighter.

Sound

The difference between the highest and lowest keys on a piano sound vastly different, but, as with vision, this represents just a fraction of the sound in which we are immersed. Remarkably, some animals have learnt to harness the extremes of pitch, from ultra-sound (squeaky high pitch) to infra-sound (booming low pitch).
Ultrasound
You may recognise the word ultrasound from doctors peering into your soft tissue - or at your growing baby - but not in the context of the animal kingdom. Bats and many other species use ultrasound to echolocate, which involves firing an astoundingly high pitched noise out into the environment.

This series of high frequency sound waves reverberates off anything it contacts, such as a tasty prey item buzzing nearby. The bat then harvests the reflected sound waves and uses them to pin point the objects around them.

Dolphins are another phenomenal species which can echolocate, and have even been observed inspecting human babies hidden inside pregnant women.
Infrasound
In stark contrast to ultrasound, the less familiar infrasound describes sound too low in pitch for humans to hear. Infrasound fills the sea with the chorus of whales as well as dominating the land with a whole host of creatures capitalising on it including elephants, giraffes and alligators.

Low pitch sounds can travel a lot further than higher pitches, so are often used by animals occupying wide open spaces, like deserts and oceans, because they allow these animals to communicate over vast distances - thousands of miles for whale calls..

Smell

With sniffer dogs able to detect anything from drugs to cancer, we humans are under no illusions that our sense of smell leaves a lot to be desired. Some animals can smell over great distances; certain species of bear can detect smells up to 20 miles away (black bear) or through nearly a metre of ice (grizzly bear).

Other animals, such as rats, are able to accurately pin-point the source of a scent due to their ability to isolate the information from each nostril, which is being used to help detect TB, cancer and even landmines.

But the species with the most intriguing sense of smell is the star nosed mole: these miraculous creatures can smell underwater. They do this by partially exhaling to hold an air bubble on the tip of their nose to absorb surrounding odours before inhaling the bubble and deciphering the scent molecules in it.

Touch

The sense of touch covers so much more than just feeling something make contact with the skin. In just a fraction of a second, touch receptors detect pressure, heat, texture, and even pain. The number of receptors in a given area dictate the sensitivity of this detection; in humans the areas with the most concentrated touch receptors are the lips and fingertips. Revisiting the incredible star nosed mole, their exquisite noses have six times as many sensory receptors than human hands.

Taste

All animals use taste to distinguish between the edible and the inedible, a vital function to avoid poison or over ingestion of certain compounds such as salt. But how do you decipher what is edible before it's too late?

Catfish have devised just the tool: their bodies are covered in taste receptors so they can tell when a tasty meal is close by. This sense is crucial for survival in the murky waters they call home. In contrast, chickens come last in the pecking order - excuse the pun - with the fewest taste buds.

Electricity

Here's one us humans are completely out of our depth at sensing. Electric eels, as the name would suggest, are famous for the high voltage that surges through them, but it may surprise you to learn that other sea creatures can sense this, including sharks and lesser prey fish.

As if sharks weren't powerful enough with their awesome jaws, lightning-fast swimming and precise sense of smell, they can also detect electricity meaning no fish is safe. Electric fields are prevalent everywhere and are distorted by movement as fine as the flexing of gills. With specialised pores filled with electro-sensitive gel, sharks can detect these changes in the electric fields to spot stealthy prey.

Super animal senses

These phenomenal ways of experiencing the world are varied and ingenious, but before we well up with envy, remember that no creature can harness the power of all of these special senses. Each species has adapted to its own ecological niche, evolving the best senses for their habitat - that is what makes the natural world so diverse and wonderful.
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Having five senses at our disposal seems great, until you realise many animals have either bettered these senses or created entirely new ways of experiencing the world around them. Here are some of the special animal senses evolved over millions of years, that give them the edge over our human senses.

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Ed Yong: Suicidal wasps, zombie roaches and other parasite tales

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Can Your Environment Affect Your DNA? | Epigenetics Explained

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A world-first study by Australian researchers has found that krill can digest certain forms of microplastic into smaller - but no less pervasive - fragments.

The study, published in Nature Communications journal on Friday, found that Antarctic krill, Euphausia superba, can break down 31.5 micron polyethylene balls into fragments less than one micron in diameter.

The study was conducted in laboratory conditions with new plastics. The lead researcher, Dr Amanda Dawson, who completed the study as part of a PhD with Griffith University, said that it was likely that microplastics in the ocean would be even easier to digest because they had already been degraded by UV radiation.

Within five days in a plastic-free environment, all plastics had left the krills' systems, meaning that microplastics from krill would not accumulate in animals further up the food chain, such as whales.

The digested fragments were on average 78% smaller than the original fragments, with some up to 94% smaller.

Unfortunately, Dawson said, krill were unlikely to provide a solution to the levels of plastics and microplastics polluting the oceans.

"It's not necessarily helping plastic pollution, it's just changing it to make it easier for small animals to eat it," she said. "It could be a new source of plastics for the deep ocean."

A study by Newcastle University in December found microplastics in the stomachs of deep-sea creatures from 11km deep trenches in the Pacific Ocean.

Dawson said microplastics that had been digested by krill were also too small to be detected in most oceanic plastic surveys, meaning the level of microplastics in the ocean could be higher than currently assumed.

Co-author Dr So Kawaguchi, a krill biologist from the Australian Antarctic Division, where the experiments were conducted, said the krill had effectively turned microplastics into nanoplastics.

"It's a new pathway for microplastics to interact with the ecosystem, and we need to learn more about how microplastics interact with the environment," Kawaguchi said.

Microplastics are fragments of less than 5mm in diameter. Krill cannot consume anything greater than 2mm in diameter.

"They are not going to be able to eat a drink bottle," Dawson said.

The plastics they do consume are broken up by the animal's gastric mill, which Dawson said functioned like a mortar and pestle.

"I would assume that other planktonic crustaceans should be able to do this as well, we just haven't seen it yet in any laboratory studies," she said.

It's not clear whether fibrous microplastics, such as fishing line or threads from clothing, can be digested in the same manner. Fibrous microplastics made up a greater proportion of the microplastics encountered by krill in the wild, Dawson said.

A global analysis conducted by US academics last year found that plastic waste was so high as to threaten a "a near permanent contamination of the natural environment".
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Krill found to break down microplastics - but it won't save the oceans

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A world-first study by Australian researchers has found that krill can digest certain forms of microplastic into smaller - but no less pervasive - fragments. The study, published in Nature Communications journal on Friday, found that Antarctic krill, Euphausia superba, can break down 31.5 micron polyethylene balls into fragments less than one micron in diameter.

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Diabetes that begins in adulthood falls into five distinct categories, new research has revealed, with scientists suggesting it is time to ditch the idea that diabetes is largely split into two types.

Researchers say all of the newly classified subgroups are genetically distinct and have numerous differences, including the age at which they tend to occur and different levels of risk for complications such as kidney disease.

The team say the findings shed light on why some diabetics respond very differently to treatment than others, adding that it could help identify those who might be at high risk of complications, and lead to tailored treatment of the disease.

"For the patient, I think it will mean a more individualised therapy [and] a better quality of life," said Leif Groop, professor of diabetes and endocrinology at Lund University, who led the study.

At present, diabetes is classified into two main forms, both of which have links to genetics. Type 1 is an autoimmune condition where the hormone insulin is not produced, and which generally develops in childhood. The more common form, type 2, in which little insulin is produced or does not trigger glucose uptake by the body's cells, generally develops later in life and is linked to obesity.

However, the latest study suggests this classification is too simplistic.

Writing in the journal The Lancet Diabetes and Endocrinology, researchers describe how they discovered the five sub-groups by analysing information from 8,980 diabetics diagnosed as adults in a Swedish registry. The results were confirmed using data from 5,795 other adult patients across another three further databases from Sweden and Finland.

The team say the findings show that type 1 diabetes and a late-onset autoimmune form of diabetes can be grouped together as one form, dubbed severe autoimmune diabetes.

However the researchers say what would generally have been called "type 2" diabetes in fact encompasses four categories, two of which are severe forms of the disease.

Traditional diabetes grouping

One, dubbed severe insulin-deficient diabetes, shows similar features to the autoimmune group such as relatively low body mass index (BMI), lack of insulin and early onset, but did not have telltale antibodies indicating an autoimmune disease. Diabetic eye disease was most common in this group.

While this group had the highest proportion of patients on the drug metformin, Groop said this was not the optimum treatment. "They clearly need insulin very soon, almost as much as 'type 1'," he said.

The other severe category, called severe insulin-resistant diabetes, is linked to obesity and shows a strong tendency for the body's cells not to respond to insulin, with these patients showing the highest likelihood of having liver disease, chronic kidney disease, and diabetic kidney disease. This group had a low proportion of patients taking metformin, although the authors say they would be expected to benefit the most from the drug.

The two other categories are mild forms of the disease with one of them, known as mild obesity-related diabetes, linked to high BMI and the other, mild age-related diabetes, generally seen in older patients. The team say both categories can be managed with metformin and lifestyle advice.

"Diabetes is not the grey mass we have been calling type 2 - there are really subsets of the disease that require different treatment," said Groop.

Proposed new categories.

The categories were discovered by considering six different metrics, including a measure of blood glucose control, age at diagnosis, BMI, the presence of certain antibodies linked to autoimmune diabetes, and a measure of insulin sensitivity.

Genetic analysis revealed that all five subgroups are genetically distinct. Researchers say the groupings held both for those with newly diagnosed diabetes and those who had long had the disease, further suggesting the five categories are not simply down to different stages of the same form of diabetes - although further work is needed to explore whether patients can move between the types. It is also not clear if the different classifications have different causes.

Dr Emily Burns, head of research communications at Diabetes UK said finding diabetes subtypes could help patients, but that more work was needed.

"This research takes a promising step toward breaking down type 2 diabetes in more detail, but we still need to know more about these subtypes before we can understand what this means for people living with the condition," she said. "For example, whether we'd find the same subtypes in people of different ethnicity or nationality."
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Five categories for adult diabetes, not just type 1 and type 2, study shows

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Diabetes that begins in adulthood falls into five distinct categories, new research has revealed, with scientists suggesting it is time to ditch the idea that diabetes is largely split into two types. Researchers say all of the newly classified subgroups are genetically distinct and have numerous differences, including the age at which they tend to occur and different levels of risk for complications such as kidney disease.

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Speciation, where one species diverges into two, is a well-known concept in the theory of evolution. But a new study based on almost 20 years of research has revealed that "speciation reversal", the merging of two previously distinct lineages, may also play an important role.

Scientists have discovered that two lineages of common raven that spent between one and two million years evolving separately appear to be in the process of such a consolidation. The findings raise intriguing questions about how science should define species - and whether the boundaries are as clearcut as once thought.

"The bottom line is [speciation reversal] is a natural evolutionary process, and it's probably happened in hundreds, or almost certainly thousands, of lineages all over the planet," said Kevin Omland, professor of biological sciences at University of Maryland, Baltimore County (UMBC) and co-author of the new study. "One of our biggest goals is to just have people aware of this process."

Omland first began studying the raven 20 years ago, after he began to suspect that two separate species could have been lumped together. He reported the existence of two lineages: one concentrated in the southwestern United States, dubbed "California," and another found everywhere else (including Maine, Alaska, Norway and Russia) called "Holarctic".

The latest paper, published in Nature Communications, provides new intriguing details of the evolutionary history of the two groups. A genetic analysis of 400 birds spanning the geographical range of the two populations suggests that the California and Holarctic lineages diverged between one and two million years ago, but more recently have merged together again and have been hybridising for at least tens of thousands of years. The two populations now comprise pure Holarctic ravens and a group that are hybrids of the two original lineages (the pure California type no longer exists).

"The extensive genetic data reveals one of the best supported examples of speciation reversal of deeply diverged lineages to date," said Arild Johnsen, professor of zoology and evolutionary biology at University of Oslo and another co-author. "The biggest thing is the degree to which we've caught them in the act."

The genetic analysis also revealed that the mitochondrial DNA of the hybrids and the Holarctics differed by about 4%, which the scientists said was twice as much as would normally be seen for birds to be considered separate species.

Despite being genetically distinct, though, the birds look the same, sound the same and behave the same - although it is possible that they were different before they started to merge into one group.

The paper also notes that a third group of ravens - known as Chihuahuan ravens - which branched off from the California lineage, have remained separate and do not interbreed with the other two groups, despite their geographical ranges overlapping. Scientists are not sure why this is the case.

"The Chihuahuan raven doesn't want to play," said Omland. "It stays by itself and doesn't interbreed with the others."

The team is now investigating what prompted the merger between the two populations, including whether humans played a role. They are analysing genetic data from ravens that lived in the early 1900s to investigate whether the hybridisation has accelerated since then.
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Two become one: two raven lineages merge in 'speciation reversal'

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Speciation, where one species diverges into two, is a well-known concept in the theory of evolution. But a new study based on almost 20 years of research has revealed that "speciation reversal", the merging of two previously distinct lineages, may also play an important role.

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Modern birds descended from a group of two-legged dinosaurs known as theropods, whose members include the towering Tyrannosaurus rex and the smaller velociraptors. The theropods most closely related to avians generally weighed between 100 and 500 pounds - giants compared to most modern birds - and they had large snouts, big teeth, and not much between the ears. A velociraptor, for example, had a skull like a coyote's and a brain roughly the size of a pigeon's.

For decades, paleontologists' only fossil link between birds and dinosaurs was archaeopteryx, a hybrid creature with feathered wings but with the teeth and long bony tail of a dinosaur. These animals appeared to have acquired their birdlike features - feathers, wings and flight - in just 10 million years, a mere flash in evolutionary time. "Archaeopteryx seemed to emerge fully fledged with the characteristics of modern birds," said Michael Benton, a paleontologist at the University of Bristol in England.

To explain this miraculous metamorphosis, scientists evoked a theory often referred to as "hopeful monsters." According to this idea, major evolutionary leaps require large-scale genetic changes that are qualitatively different from the routine modifications within a species. Only such substantial alterations on a short timescale, the story went, could account for the sudden transformation from a 300-pound theropod to the sparrow-size prehistoric bird Iberomesornis.

But it has become increasingly clear that the story of how dinosaurs begat birds is much more subtle. Discoveries have shown that bird-specific features like feathers began to emerge long before the evolution of birds, indicating that birds simply adapted a number of pre-existing features to a new use. And recent research suggests that a few simple changes - among them the adoption of a more babylike skull shape into adulthood - likely played essential roles in the final push to bird-hood. Not only are birds much smaller than their dinosaur ancestors, they closely resemble dinosaur embryos. Adaptations such as these may have paved the way for modern birds' distinguishing features, namely their ability to fly and their remarkably agile beaks. The work demonstrates how huge evolutionary changes can result from a series of small evolutionary steps.

A Phantom Leap

In the 1990s, an influx of new dinosaur fossils from China revealed a feathery surprise. Though many of these fossils lacked wings, they had a panoply of plumage, from fuzzy bristles to fully articulated quills. The discovery of these new intermediary species, which filled in the spotty fossil record, triggered a change in how paleontologists conceived of the dinosaur-to-bird transition. Feathers, once thought unique to birds, must have evolved in dinosaurs long before birds developed.

Sophisticated new analyses of these fossils, which track structural changes and map how the specimens are related to each other, support the idea that avian features evolved over long stretches of time. In research published in Current Biology last fall, Stephen Brusatte, a paleontologist at the University of Edinburgh in Scotland, and collaborators examined fossils from coelurosaurs, the subgroup of theropods that produced archaeopteryx and modern birds. They tracked changes in a number of skeletal properties over time and found that there was no great jump that distinguished birds from other coelurosaurs.

"A bird didn't just evolve from a T. rex overnight, but rather the classic features of birds evolved one by one; first bipedal locomotion, then feathers, then a wishbone, then more complex feathers that look like quill-pen feathers, then wings," Brusatte said. "The end result is a relatively seamless transition between dinosaurs and birds, so much so that you can't just draw an easy line between these two groups."

Yet once those avian features were in place, birds took off. Brusatte's study of coelurosaurs found that once archaeopteryx and other ancient birds emerged, they began evolving much more rapidly than other dinosaurs. The hopeful monster theory had it almost exactly backwards: A burst of evolution didn't produce birds. Rather, birds produced a burst of evolution. "It seems like birds had happened upon a very successful new body plan and new type of ecology - flying at small size - and this led to an evolutionary explosion," Brusatte said.

The Importance of Being Small

Though most people might name feathers or wings as a key characteristic distinguishing birds from dinosaurs, the group's small stature is also extremely important. New research suggests that bird ancestors shrank fast, indicating that the diminutive size was an important and advantageous trait, quite possibly an essential component in bird evolution.

Like other bird features, diminishing body size likely began long before the birds themselves evolved. A study published in Science last year found that the miniaturization process began much earlier than scientists had expected. Some coelurosaurs started shrinking as far back as 200 million years ago - 50 million years before archaeopteryx emerged. At that time, most other dinosaur lineages were growing larger. "Miniaturization is unusual, especially among dinosaurs," Benton said.

That shrinkage sped up once bird ancestors grew wings and began experimenting with gliding flight. Last year, Benton's team showed that this dinosaur lineage, known as paraves, was shrinking 160 times faster than other dinosaur lineages were growing. "Other dinosaurs were getting bigger and uglier while this line was quietly getting smaller and smaller," Benton said. "We believe that marked an event of intense selection going on at that point."

The rapid miniaturization suggests that smaller birds must have had a strong advantage over larger ones. "Maybe this decrease was opening up new habitats, new ways of life, or even had something to do with changing physiology and growth," Brusatte said. Benton speculates that the advantage of being pint-size might have emerged as bird ancestors moved to trees, a useful source of food and shelter.

But whatever the reasons may be, small stature was likely a useful precursor to flight. Though larger animals can glide, true flight powered by beating wings requires a certain ratio of wing size to weight. Birds needed to become smaller before they could ever take to the air for more than a short glide.

Baby Face

In 2008, Arkhat Abzhanov, a biologist at Harvard University, was elbow deep in alligator eggs. Since alligators descend from a common ancestor with dinosaurs, they can provide a useful evolutionary comparison to birds. (Despite their appearance, birds are more closely related to alligators than lizards are.) Abzhanov was studying alligators' vertebrae, but what struck him most was the birdlike shape of their heads; alligator embryos looked quite similar to chickens. Fossilized skulls of baby dinosaurs show the same pattern - they resemble adult birds. With those two observations in mind, Abzhanov had an idea. Perhaps birds evolved from dinosaurs by arresting their pattern of development early on in life.

To test that theory, Abzhanov, along with Mark Norell, a paleontologist at the American Museum of Natural History in New York, Bhart-Anjan Bhullar, then a doctoral student in Abzhanov's lab, and other colleagues, collected data on fossils from around the globe, including ancient birds, such as archaeopteryx, and fossilized eggs of developing dinosaurs that died in the nest. They tracked how the skull shape changed as dinosaurs morphed into birds.

Over time, they discovered, the face collapsed and the eyes, brain and beak grew. "The first birds were almost identical to the late embryo from velociraptors," Abzhanov said. "Modern birds became even more babylike and change even less from their embryonic form." In short, birds resemble tiny, infantile dinosaurs that can reproduce.

This process, known as paedomorphosis, is an efficient evolutionary route. "Rather than coming up with something new, it takes something you already have and extends it," said Nipam Patel, a developmental biologist at the University of California, Berkeley.

"We're seeing more and more that evolution operates much more elegantly than we previously appreciated," said Bhullar, who will start his own lab at Yale University in the fall. "The umpteen changes that go into the bird skull may all owe to paedomorphosis, to one set of molecular changes in the early embryo."

Why would paedomorphosis be important for the evolution of birds? It might have helped drive miniaturization or vice versa. Changes in size are often linked to changes in development, so selection for small size may have arrested the development of the adult form. "A neat way to cut short a developmental sequence is to stop growing at smaller size," Benton said. A babylike skull in adults might also help explain birds' increased brain size, since baby animals generally have larger heads relative to their bodies than adults do. "A great way to improve brain size is to retain child size into adulthood," he said.

(Indeed, paedomorphosis might underlie a number of major transitions in evolution, perhaps even the development of mammals and humans. Our large skulls relative to those of chimpanzees could be a case of paedomorphosis.)

What's more, paedomorphosis helped to make the skull a blank slate on which selection could create new structures. By erasing the snout, it may have paved the way for another of birds' most important features: the beak.

Birth of the Beak

The problem with studying something that occurred deep in evolutionary time is that it's impossible to know exactly what happened. Scientists can never precisely decipher how birds evolved from dinosaurs or which set of features was essential for that transformation. But with the intersection of three fields - evolution, genetics and developmental biology - they can now begin to explore how specific features might have come about.

One of Abzhanov's particular interests is the beak, a remarkable structure that birds use to find food, clean themselves, make nests, and care for their young. He theorizes that birds' widespread success stems not just from their ability to fly, but from their amazing diversity of beaks. "Modern birds evolved a pair of fingers on the face," he said.

Armed with their insight into bird evolution, Abzhanov, Bhullar and collaborators have been able to dig into the genetic mechanisms that helped form the beak. In new research, published last month in , the researchers show that just a few small genetic tweaks can morph a bird face into one that resembles a dinosaur.

In modern birds, two bones known as the premaxillary bones fuse to become the beak. That structure is quite distinct from that of dinosaurs, alligators, ancient birds and most other vertebrates, in which these two bones remain separate, shaping the snout. To figure out how that change might have arisen, the researchers mapped out the activity of two genes that are expressed in these bones in a spectrum of animals: alligators, chickens, mice, lizards, turtles and emus, a living species reminiscent of ancient birds.

They found that the reptiles and mammals had two patches of activity, one on either side of the developing nasal cavity. Birds, on the hand, had a much larger single patch spanning the front of the face. The researchers reasoned that the alligator pattern could serve as a proxy for that of dinosaurs, given that they have similar snouts and premaxillary bones. The researchers then undid a bird-specific pattern of gene expression in chicken embryos using chemicals to block the genes in the middle of the face. (For ethical reasons, they did not allow the chickens to hatch.)

The result: The treated embryos developed a more dinosaurlike face. "They basically grew a bird embryo back into something that looked more like the morphology of extinct dinosaurs," said Timothy Rowe, a paleontologist at the University of Texas, Austin, who has previously collaborated with Abzhanov.

The findings highlight how simple molecular tweaks can trigger major structural changes. Birds "use existing tools in a new way to create a whole new face," Abzhanov said. "They didn't evolve a new gene or pathway, they just changed control of an existing gene."

Like the studies of Brusatte and others, Abzhanov's work challenges the hopeful monster theory, and it does so on a genetic scale. The creation of the beak didn't require some special evolutionary jump or large-scale genetic changes. Rather, Abzhanov showed that the same forces that shape microevolution - minor alterations within species - also drive macroevolution, the evolution of whole new features and new groups of species.

Specifically, small changes in how genes are regulated likely drove both the initial creation of the beak, which evolved over millions of years, and the diverse shape of bird beaks, which can change over just a few generations. "We show that simple regulatory changes can have a major impact," Abzhanov said.

Bhullar and Abzhanov plan to dig deeper into the question of how the beak and bird skull evolved, using the same approach to manipulate different features of skull and brain development. "We have just scratched surface of this work," Bhullar said.
Correction June 3, 2015: The original article stated that alligators descended from dinosaurs. In fact, alligators and dinosaurs share a common ancestor. The article has been revised to reflect this. June 4, 2015: The dinosaur silhouettes in "The Incredible Shrinking Bird" graphic are based on the following illustrations: Monolophosaurus by Jordan Mallon, Deinonychus by Emily Willoughby, and Velociraptor by Matt Martyniuk. This article was reprinted on ScientificAmerican.com.

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How Birds Evolved From Dinosaurs | Quanta Magazine

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Modern birds descended from a group of two-legged dinosaurs known as theropods, whose members include the towering Tyrannosaurus rex and the smaller velociraptors. The theropods most closely related to avians generally weighed between 100 and 500 pounds - giants compared to most modern birds - and they had large snouts, big teeth, and not much between the ears.

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How Animals Behave, Series 17, The Infinite Monkey Cage - BBC Radio 4

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Brian Cox and Robin Ince are joined by Rufus Hound to look at animal behaviour.

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Podcast:The secret life of bird - infinite monkey cage

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Podcast:The secret life of bird - infinite monkey cage

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http://www.bbc.co.uk/programmes/b09ly26f

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The Secret Life of Birds, Series 17, The Infinite Monkey Cage - BBC Radio 4

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Brian Cox and Robin Ince explore the secret life of birds.

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Despite What You Learned in School, Tongue Rolling ... - Curiosity

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The lake is basic. The slippery, scuba-diving fly that lives there is not. - Popular Science

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The lake is basic. The slippery, scuba-diving fly that lives there is not. - Popular Science

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The lake is basic. The slippery, scuba-diving fly that lives there is not. - Popular Science

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There was a salty lake that swallowed a fly. I do know why it swallowed the fly, and rest assured, neither the lake nor the fly is going to die any sooner as a result.

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Watch: Biology Student Raps About Cell Division in Excellent Viral Video - Newsweek

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Watch: Biology Student Raps About Cell Division in Excellent Viral Video - Newsweek

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Watch: Biology Student Raps About Cell Division in Excellent Viral Video - Newsweek

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This Morehouse College student is having a moment.

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A new magic wand for stem cell scientists - Stem Cell News

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A new magic wand for stem cell scientists - Stem Cell News

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A new magic wand for stem cell scientists - Stem Cell News

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By harnessing massive amounts of data on activity within and between snippets of DNA, US scientists found the algorithm for transforming any cell into any other type. Researchers say it could be possible to reprogram both healthy and diseased cells. In fairy tales, all it takes to transform a frog into a prince, a...

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British scientists have worked out how many changes it takes to transform a healthy cell into a cancer.

The team, at the Wellcome Trust Sanger Institute, showed the answer was a tiny handful, between one and 10 mutations depending on the type of tumour.

It has been one of the most hotly debated issues in cancer science for decades.

The findings, published in the journal Cell, could improve treatment for patients.

If you played spot the difference between a cancer and healthy tissue, you could find tens of thousands of differences - or mutations - in the DNA.

Some are driving the cancer's growth, while others are just along for the ride. So which ones are important?

Root cause

The researchers analysed the DNA from 7,664 tumours to find "driver mutations" that allow a cell to be more selfish, aggressive and cancerous.

They showed it could take:

just one mutation to drive thyroid and testicular cancers

four mutations to make a breast or liver cancer

10 mutations to create a colorectal cancer.

Dr Peter Campbell, one of the researchers, told the BBC News website: "We've known about the genetic basis of cancer for many decades now, but how many mutations are responsible has been incredibly hotly debated.

"What we've been able to do in this study is really provide the first unbiased numbers.

"And it seems that of the thousands of mutations in a cancer genome, only a small handful are responsible for dictating the way the cell behaves, what makes it cancerous."

Half the mutations identified were in sets of genetic instructions - or genes - that had never been implicated in cancer before.

Therapy

The long-term goal is to advance precision cancer treatment.

If doctors know which few mutations, out of thousands, were driving a patient's cancer, it could allow drugs that specifically targeted that mutation to be used.

Drugs such as herceptin and Braf inhibitors are already used to attack specific mutations in tumours.

The researchers were able to pick out the mutations that were driving the growth of cancer by turning to Charles Darwin and evolutionary theory.

In essence, driver mutations should appear more often in tumours than "neutral" mutations that do not make the cell cancerous.

This is because the forces of natural selection give an evolutionary advantage to mutations that help a cell grow and divide more readily.

Dr Nicholas McGranahan, from the Cancer Research UK and the UCL Cancer Institute, said the approach was "elegant".

He said: "Cancer is a disease that evolves and changes over time, and it makes sense to use ideas like this from species evolution to work out the genetic faults that cause cancer to grow.

"But as this study focuses on one part of cancer evolution, it can only give us insight into part of the puzzle.

"Other components such as how DNA is packaged into chromosomes are also key in how a tumour progresses and will need to be looked at to give us a clearer picture of how cancer evolves."

Follow James on Twitter.

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British scientists have worked out how many changes it takes to transform a healthy cell into a cancer. The team, at the Wellcome Trust Sanger Institute, showed the answer was a tiny handful, between one and 10 mutations depending on the type of tumour.

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David Attenborough urges action on plastics after filming Blue Planet II

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David Attenborough urges action on plastics after filming Blue Planet II

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Sir David Attenborough has urged the world to cut down on the use of plastics by "tomorrow" to curb increasing dangers to the ocean.

The TV naturalist told how his experience filming the second Blue Planet series demonstrated to him the threat that plastic causes to the underwater environment.

His comments came as he attended a question and answer session about the show ahead of its broadcast on BBC One later this month, 15 years after the original series.

Asked what concerned him the most about the crew's findings, the 91-year old said: "Two things. One of course is the rising temperature, and particularly in the last programme it is illustrated what happens if the temperature goes up by 1.5 degrees.

"The second thing is plastic. Plastic in the ocean. Now, what we're going to do about 1.5 degrees rise in the temperature of the ocean over the next 10 years, I don't know, but we could actually do something about plastic right now. And I just wish we would.

"There are so many sequences that every single one of us have been involved in, even in the most peripheral way, where we have seen tragedies happen because of the plastic in the ocean. We've seen albatross come back with their belly full of food for their young and nothing in it.

"The albatross parent has been away for three weeks gathering stuff for her young and what comes out? What does she give her chick? You think it's going to be squid, but it's plastic. And the chick is going to starve and die.

"There are more examples of that. But we could do things about plastic internationally tomorrow."

Explaining how he hoped the programme would encourage viewers to think about our impact on the environment, he continued: "We have a responsibility. Every one of us. We may think we live a long way from the oceans but we don't.

"What we actually do here, and in the middle of Asia and wherever has a direct effect on the oceans and what the oceans do, then reflects back on us.

"It is one world. And it's in our care. For the first time in the history of humanity, for the first time in 500m years, one species has the future in the palm of its hands. I just hope he realises that that is the case."

Attenborough, who presents Blue Planet II, appeared on the Q&A panel with composer Hans Zimmer, executive producer James Honeyborne, series producer Mark Brownlow and producer Orla Doherty before the programme's broadcast this month.

The programme is a a BBC Studios Natural History Unit production and filming took place all over the world, in locations including South Africa, Egypt, Australia, Mexico, Japan and Norway. It will air on 29 October.

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David Attenborough urges action on plastics after filming Blue Planet II

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Sir David Attenborough has urged the world to cut down on the use of plastics by "tomorrow" to curb increasing dangers to the ocean. The TV naturalist told how his experience filming the second Blue Planet series demonstrated to him the threat that plastic causes to the underwater environment.

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Magic mushrooms can 'reset' depressed brain

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Magic mushrooms can 'reset' depressed brain

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A hallucinogen found in magic mushrooms can "reset" the brains of people with untreatable depression, raising hopes of a future treatment, scans suggest.

The small study gave 19 patients a single dose of the psychedelic ingredient psilocybin.

Half of patients ceased to be depressed and experienced changes in their brain activity that lasted about five weeks.

However, the team at Imperial College London says people should not self-medicate.

There has been a series of small studies suggesting psilocybin could have a role in depression by acting as a "lubricant for the mind" that allows people to escape a cycle of depressive symptoms.

But the precise impact it might be having on brain activity was not known.

The team at Imperial performed fMRI brain scans before treatment with psilocybin and then the day after (when the patients were "sober" again).

The study, published in the journal Scientific Reports, showed psilocybin affected two key areas of the brain.

The amygdala - which is heavily involved in how we process emotions such as fear and anxiety - became less active. The greater the reduction, the greater the improvement in reported symptoms.

The default-mode network - a collaboration of different brain regions - became more stable after taking psilocybin.

Dr Robin Carhart-Harris, head of psychedelic research at Imperial, said the depressed brain was being "clammed up" and the psychedelic experience "reset" it.

He told the BBC News website: "Patients were very ready to use this analogy. Without any priming they would say, 'I've been reset, reborn, rebooted', and one patient said his brain had been defragged and cleaned up."

However, this remains a small study and had no "control" group of healthy people with whom to compare the brain scans.

Further, larger studies are still needed before psilocybin could be accepted as a treatment for depression.

However, there is no doubt new approaches to treatment are desperately needed.

Prof Mitul Mehta, from the Institute of Psychiatry at King's College London, said: "What is impressive about these preliminary findings is that brain changes occurred in the networks we know are involved in depression, after just a single dose of psilocybin.

"This provides a clear rationale to now look at the longer-term mechanisms in controlled studies."

Follow James on Twitter.

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A hallucinogen found in magic mushrooms can "reset" the brains of people with untreatable depression, raising hopes of a future treatment, scans suggest. The small study gave 19 patients a single dose of the psychedelic ingredient psilocybin. Half of patients ceased to be depressed and experienced changes in their brain activity that lasted about five weeks.

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Female dolphins evolved protective vaginas to stop unwanted males mating with them - The Independent

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Female dolphins evolved protective vaginas to stop unwanted males mating with them - The Independent

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Female dolphins evolved protective vaginas to stop unwanted males mating with them - The Independent

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Female bottlenose dolphins have evolved to the point where they are able to protect themselves from fertilisation by some males.

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New Stem Cell Line Could Open New Doors in Medical Research and Treatment - Futurism

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New Stem Cell Line Could Open New Doors in Medical Research and Treatment - Futurism

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New Stem Cell Line Could Open New Doors in Medical Research and Treatment - Futurism

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There's a new type of stem cell line available, at least in mice. Researchers from the Wellcome Trust Sanger Institute and their partners have developed stem cells from the earliest possible development stage in cells.

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Inside Cells, Genetic War Could Create New Species - WIRED

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Inside Cells, Genetic War Could Create New Species - WIRED

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Inside Cells, Genetic War Could Create New Species - WIRED

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Mitonuclear conflict-a struggle between the genes in a cell's nucleus and those in its mitochondria-might sometimes split species in two.

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The blueprint for life - DNA - has been altered in human embryos for the first time in the UK.

The team at the Francis Crick Institute are unravelling the mysteries of the earliest moments of life.

Understanding what happens after a sperm fertilises an egg could lead to ways of improving IVF or explain why some women miscarry.

The embryos were modified shortly after fertilisation and allowed to develop for seven days.

The researchers are exploring one of the most astounding of transformations.

We have all journeyed from a single fertilised egg to a human being - built from myriad different tissues ranging from bone to those needed to read this page.

The first few steps on that journey are as critical as they are poorly understood.

Breakthroughs in manipulating DNA have allowed the team at the Crick to turn off a gene - a genetic instruction - suspected to be of vital importance.

The easiest way of working out how something works is to remove it and see what happens.

So the researchers used the gene-editing tool Crispr-Cas9 to scour the billions of letters of genetic code, find their genetic target and break the DNA to effectively disable it.

They were targeting a gene. You are unlikely to have heard of it, but OCT4 is a superstar in early embryo development.

Its complete role is not understood but it acts like an army general issuing commands to keep development on track.

The researchers used 41 embryos that had been donated by couples who no longer needed them for IVF.

After performing the genetic modification, the team could watch how the embryos developed without OCT4.

Over the course of the first seven days, a healthy, normal embryo goes from one cell to about 200. It also goes through the first steps of organising itself and handing out specialised jobs to different cells.

The embryo forms a hollow sphere called a blastocyst, with some cells destined to go on to form the placenta, some the yolk sac and others, ultimately, us.

But without OCT4 the blastocyst cannot form. It tries - but implodes in on itself.

From the embryo's perspective it is a disaster but for scientists it has given unprecedented insight.

It is the first time human embryos have been edited to answer questions about fundamental biology.

Dr Kathy Niakan, a group leader at the Crick in London, told the BBC: "When it seemed it was working we were quite excited about the possibility that this would open up.

"This is basic research which is providing us with a foundation of knowledge about early human development."

By deepening understanding of the earliest moments in life, it could help explain what goes wrong in infertility.

During IVF, of 100 fertilised eggs, fewer than 50 reach the blastocyst stage, 25 implant into the womb and only 13 develop beyond three months.

This study alone, published in the journal Nature, cannot explain what is going wrong or why some women miscarry.

But by interrogating all the genes suspected of playing a role in our inception, it could lead to new advances.

Dr Niakan told the BBC: "If we knew the key genes for an embryo to develop successfully that would, I would hope in the future, lead to improvements in IVF technology and give us really important insights into why some pregnancies fail."

One option for IVF is to have a better way of testing which embryos are going to be successful.

Or it may be possible to boost embryos during IVF by growing them in a different culture media - a fertiliser for fertilised eggs.

Ethical debate

These experiments have been legal since 2008 in the UK, where it is possible to manipulate such embryos for 14 days as long as they are not implanted.

But while this application of the technology is answering fundamental questions of science, other research groups are trying to remove genes that cause disease.

That is provoking deep ethical debate.

Dr Sarah Chan, a bioethicist at the University of Edinburgh, told the BBC: "I don't think this study should raise any ethical concerns.

"It is very clear that the aim of the research was basic science and that there was never any intention to create genetically modified human beings.

"That said if we could one day use gene editing in human embryos for medical purposes, the potential benefits could be huge, but before we took such a step we would want to make sure that we'd had a really robust and wide-ranging public dialogue on all of the ethical issues involved."

Dr Rob Buckle, the chief science officer at the UK Medical Research Council, said: "Genome editing technologies are having a game-changing effect on our ability to understand the function of critical human genes.

"As genome editing techniques develop it's vital that this work continues within a robust yet adaptable regulatory framework so that its full potential can be realised in a scientific, ethical and legally rigorous way."

Follow James on Twitter.

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The blueprint for life - DNA - has been altered in human embryos for the first time in the UK. The team at the Francis Crick Institute are unravelling the mysteries of the earliest moments of life. Understanding what happens after a sperm fertilises an egg could lead to ways of improving IVF or explain why some women miscarry.

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Researchers Have Discovered a New Type of Cell That Helps Our Lungs Fight Infections - Futurism

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Researchers Have Discovered a New Type of Cell That Helps Our Lungs Fight Infections - Futurism

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Researchers Have Discovered a New Type of Cell That Helps Our Lungs Fight Infections - Futurism

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New research indicates that a gene previously believed to only be expressed in germ cells is also expressed in a certain type of lung cell. These cells play an important role in our bodies' ability to naturally defend against infections, so this new discovery could lead to novel therapeutic strategies.

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Scientists Can Now Repaint Butterfly Wings - The Atlantic

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Scientists Can Now Repaint Butterfly Wings - The Atlantic

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Scientists Can Now Repaint Butterfly Wings - The Atlantic

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Thanks to CRISPR, scientists are studying animal evolution in ways that were previously thought to be impossible.

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A handheld device can identify cancerous tissue in 10 seconds, according to scientists at the University of Texas.

They say it could make surgery to remove a tumour quicker, safer and more precise.

And they hope it would avoid the "heartbreak" of leaving any of the cancer behind.

Tests, published in Science Translational Medicine, suggest the technology is accurate 96% of the time.

The MasSpec Pen takes advantage of the unique metabolism of cancer cells.

Their furious drive to grow and spread means their internal chemistry is very different to that of healthy tissue.

How it works

The pen is touched on to a suspected cancer and releases a tiny droplet of water.

Chemicals inside the living cells move into the droplet, which is then sucked back up the pen for analysis.

The pen is plugged into a mass spectrometer - a piece of kit that can measure the mass of thousands of chemicals every second.

It produces a chemical fingerprint that tells doctors whether they are looking at healthy tissue or cancer.

The challenge for surgeons is finding the border between the cancer and normal tissue.

In some tumours it is obvious, but in others the boundary between healthy and diseased tissue can be blurred.

The pen should help doctors ensure none of the cancer is left behind.

Remove too little tissue, and any remaining cancerous cells will grow into another tumour. But take too much, and you can cause damage, particularly in organs such as the brain.

Livia Eberlin, an assistant professor of chemistry at the University of Texas, Austin, told the BBC: "What's exciting about this technology is how clearly it meets a clinical need.

"The tool is elegant and simple and can be in the hands of surgeons in a short time."

Trials

The technology has been tested on 253 samples as part of the study. The plan is to continue testing to refine the device before trialling it during operations next year.

The pen currently analyses a patch of tissue 1.5mm (0.06in) across, but the researchers have already developed pens that are even more refined and should be able to look at a finer patch of tissue just 0.6mm across.

While the pen itself is cheap, the mass spectrometer is expensive and bulky.

Dr Eberlin said: "The roadblock is the mass spectrometer, for sure.

"We're visioning a mass spectrometer that's a little smaller, cheaper and tailored for this application that can be wheeled in and out of rooms."

Dr James Suliburk, one of the researchers and the head of endocrine surgery at Baylor College of Medicine, said: "Any time we can offer the patient a more precise surgery, a quicker surgery or a safer surgery, that's something we want to do.

"This technology does all three."

The MasSpec Pen is the latest attempt to improve the accuracy of surgery.

A team at Imperial College London have developed a knife that "smells" the tissue it cuts to determine whether it is removing cancer.

And a team at Harvard are using lasers to analyse how much of a brain cancer to remove.

Dr Aine McCarthy, from Cancer Research UK, said: "Exciting research like this has the potential to speed up how quickly doctors can determine if a tumour is cancerous or not and learn about its characteristics.

"Gathering this kind of information quickly during surgery could help doctors match the best treatment options for patients sooner."

Follow James on Twitter.

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'Pen' identifies cancer in 10 seconds - BBC News

# data[].attributes.attachment_link.description
A handheld device can identify cancerous tissue in 10 seconds, according to scientists at the University of Texas. They say it could make surgery to remove a tumour quicker, safer and more precise. And they hope it would avoid the "heartbreak" of leaving any of the cancer behind.

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http://gizmodo.com/cuckoos-are-even-bigger-assholes-than-we-realized-1800009969?utm_campaign=socialflow_gizmodo_twitter&utm_source=gizmodo_twitter&utm_medium=socialflow

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Researchers Probe Protein Diversity - Science & Technology Research News

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Researchers Probe Protein Diversity - Science & Technology Research News

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Researchers Probe Protein Diversity - Science & Technology Research News

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Proteins make up a wildly diverse class of molecule, with key roles in everything from catalyzing reactions to helping fight off infection to transporting oxygen through the body. Now, Harvard scientists are beginning to provide answers on drivers of that diversity. Led by Eugene Shakhnovich, a professor of chemistry and chemical biology, and Amy Gilson,...

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A Crack in Creation review – Jennifer Doudna, Crispr and a great scientific breakthrough - the guardian

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A Crack in Creation review – Jennifer Doudna, Crispr and a great scientific breakthrough - the guardian

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A Crack in Creation review - Jennifer Doudna, Crispr and a great scientific breakthrough (the guardian)

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This is an invaluable account, by Doudna and Samuel Sternberg, of their role in the revolution that is genome editing

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Vaccines of the future could be as contagious as viruses - Popular Science

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Vaccines of the future could be as contagious as viruses - Popular Science

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Vaccines of the future could be as contagious as viruses (Popular Science)

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Scientists are taking a leaf from the virus playbook and devising vaccines and antiviral therapies that can spread from host to host.

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Routine genomic testing is feasible, but only a subset of patients benefit - Science Magazine

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Routine genomic testing is feasible, but only a subset of patients benefit - Science Magazine

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Routine genomic testing is feasible, but only a subset of patients benefit (Science Magazine)

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ASCO Perspective "This study gives more validation for the use of genomics in clinical practice and shows it could very well guide treatment choices for patients with advanced cancer," said Sumanta K..

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'Hail Mary' Mechanism Can Rescue Cells with Severely Damaged Chromosomes, Researchers Say - Scicasts

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'Hail Mary' Mechanism Can Rescue Cells with Severely Damaged Chromosomes, Researchers Say - Scicasts

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'Hail Mary' Mechanism Can Rescue Cells with Severely Damaged Chromosomes, Researchers Say (Scicasts)

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Santa Cruz, CA (Scicasts) - The DNA vital to the life of a cell is packaged in chromosomes, and a variety of checkpoints, repair mechanisms, and other cellular safeguards exist to maintain the integrity of the chromosomes during cell growth and division.

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Newly Discovered DNA Sequences Can Protect Chromosomes in Rotifers, Says Study - Scicasts

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Newly Discovered DNA Sequences Can Protect Chromosomes in Rotifers, Says Study - Scicasts

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Newly Discovered DNA Sequences Can Protect Chromosomes in Rotifers, Says Study (Scicasts)

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Woods Hole, MA (Scicasts) - Rotifers are tough, microscopic organisms highly resistant to radiation and repeated cycles of dehydration and rehydration. Now Irina Arkhipova, Irina Yushenova, and Fernando Rodriguez of the Marine Biological Laboratory (MBL) have discovered another protective mechanism of this hardy organism: the Terminons.

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Enzymes Engineered Using Direct Evolution - Science & Technology Research News

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Enzymes Engineered Using Direct Evolution - Science & Technology Research News

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Enzymes Engineered Using Direct Evolution (Science & Technology Research News)

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Organic molecules containing a fluorine atom are widely used in the materials, agrochemical and pharmaceutical industries. However, synthesizing the carbon-fluorine bond typically utilizes toxic metal catalysts and requiresanhydrous conditions and high temperatures. Now an international team has developed a milder, more efficient enzyme-based approach to create this bond1.

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It turns out that we may have more than five basic tastes - Quartz

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It turns out that we may have more than five basic tastes - Quartz

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It turns out that we may have more than five basic tastes (Quartz)

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Mammals need water to survive, so it makes sense that they may be designed with a special taste for H2O. Though water doesn't seem to...

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This map will help biologists learn more about the human body than ever before - STAT

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This map will help biologists learn more about the human body than ever before - STAT

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This map will help biologists learn new details about the human body (STAT)

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The Human Cell Atlas project, which aims to define all the cells in the human body based on the molecules they make, could transform biology and medicine.

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Whales today are bigger than ever before. Now, we know why. - Popular Science

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Whales today are bigger than ever before. Now, we know why. - Popular Science

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Whales today are bigger than ever before. Now, we know why. (Popular Science)

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Baleen whales grew into giants only recently. Read on.

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Octopuses can defy their genetic instructions – and it’s slowed down their evolution - Cosmos Magazine

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Octopuses can defy their genetic instructions – and it’s slowed down their evolution - Cosmos Magazine

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Octopuses can defy their genetic instructions - and it's slowed down their evolution (Cosmos Magazine)

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Are octopuses so clever because they ignore their genetic programming?

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21 Optical Illusions That Prove Your Brain Sucks - PC Magazine

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21 Optical Illusions That Prove Your Brain Sucks - PC Magazine

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21 Optical Illusions That Prove Your Brain Sucks (PC Magazine)

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Back in 2015, the nation-nay THE WORLD-came together to furiously debate an issue that would have-until very recently-been considered completely absurd: What color is this dress? Is it blue and black or white and gold? To me, it's obviously blue and black. But apparently, only about half the internet agrees with me.

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Skin stem cells could generate new brain cells - Knowridge

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Skin stem cells could generate new brain cells - Knowridge

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Skin stem cells could generate new brain cells | Knowridge Science Report (Knowridge)

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Using human skin cells, University of California, Irvine neurobiologists and their colleagues have created a method to generate one of the principle cell types of the brain called microglia. This type of cells plays a key role in preserving the function of neural networks and responding to injury and disease.

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Why do animal's have different life spans?

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Why do animal's have different life spans?

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Why do animals have such different lifespans? - Joao Pedro de Magalhaes

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Our ancestors defeated a virus from the same family as HIV 11 million years ago - International Business Times, UK Edition

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Our ancestors defeated a virus from the same family as HIV 11 million years ago - International Business Times, UK Edition

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Our ancestors defeated a virus from the same family as HIV 11 million years ago (International Business Times, UK Edition)

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Scientists studied ''viral fossils'' to find out how how the HERV-T retrovirus went extinct.

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Unfaithful Birds Reveal Tinder’s Evolutionary Downside - Inverse

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Unfaithful Birds Reveal Tinder’s Evolutionary Downside - Inverse

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Unfaithful Birds Reveal Tinder's Evolutionary Downside (Inverse)

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A new study suggests that polygamy unexpectedly slows down evolution's speciation process.

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What Dung Beetles Can Teach Us About Sexual Difference - Smithsonian

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What Dung Beetles Can Teach Us About Sexual Difference - Smithsonian

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What Dung Beetles Can Teach Us About Sexual Difference - Smithsonian

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When it comes to sex appeal, it's not all in your genes (it's also in your proteins!)

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An Interview With James Gathany, the CDC's Scientific Photographer - The Atlantic

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An Interview With James Gathany, the CDC's Scientific Photographer - The Atlantic

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An Interview With James Gathany, the CDC's Scientific Photographer - The Atlantic

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An interview with the CDC's scientific photographer

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Research suggests amygdala neural circuits drive pleasure-inducing behavior - PsyPost

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Research suggests amygdala neural circuits drive pleasure-inducing behavior - PsyPost

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Research suggests amygdala neural circuits drive pleasure-inducing behavior - PsyPost

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Scientists have long believed that the central amygdala, a structure located deep within the brain, is linked with fear and responses to unpleasant events. However, a team of MIT neuroscientists has now discovered a circuit in this structure that responds to rewarding events. In a study of mice, activating this circuit with certain stimuli made...

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Gut bacteria play a role in long-term weight gain

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Gut bacteria play a role in long-term weight gain

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Weight gain happens when we consume more food than we can burn, and weight loss happens when we burn more energy than we consume. But why do some people seem to eat whatever they want and not gain weight, and others appear to gain weight even if they eat reasonable amounts of food? The answer, at least in part, may be found in the bacteria that live in our guts.

Our latest research, published in the International Journal of Obesity, shows that people who have a stable weight over nine years or lose weight, have a larger number of different types of microbes in their guts, eat more fibre and have a higher abundance of certain types of gut microbes.

In the past decade, researchers have found that the microbes in our gut have a strong effect on various aspects of our health. Studies in mice have demonstrated that how the body converts food into energy depends in large part on the different types of microbes a person has in their gut and also on the kind of microbes they carry.

In a recent study, scientists in Israel found that mice who were put on a yo-yo diet slowly gained weight compared with mice on a steady diet - despite the fact that both groups received the same amount of calories overall.

One of the effects seen in the mice that were put on the yo-yo diet was a decrease in their gut microbiome diversity. Also, when they transplanted the microbes from the yo-yo dieters into the guts of non-yo-yo dieters, the mice on steady diets gained weight - showing that the altered microbes were the cause of the weight gain. But is this relevant to humans?

In humans, comparing microbes in the gut in obese and thin individuals, scientists have already shown that lean people have many more species of intestinal bacteria than obese people.

Janson George/Shutterstock.com

What twins taught us

Until now, however, there were no experiments tying the gut microbes to changes in weight over several years. For this reason, we decided to do an investigation into 1,632 women from the UK, all of them twins (about half of them identical). The participants had their body weight measured several years ago and, back then, they answered questions about the amounts and types of foods that they ate. We called them again nine years later and, in addition to measuring their weight, we asked them to give us a poo sample so we could analyse the bacteria in their gut.

We found that most of the women gained weight over the nine years, but this was not fully explained by the number of calories in their diet when the study began. Because they are twins, it was also possible to calculate (using the differences between identical and non-identical twins) how much of the weight gain can be explained by genes. Only 41% of the change in weight was explained by genes. That meant that there were other factors, in addition to genes and calories.

We discovered that women who ate high amounts of dietary fibre (found in fruit, vegetables and whole grains) were less likely to gain weight than those who ate little fibre, even if they consumed roughly the same amount of calories. Women who lost weight or had stable weight also had more diverse microbes in their guts. We were able to pinpoint some of the microbes that are different between women who had gained weight and those who had lost weight. Most of these microbes had already been discovered in mice to be involved in better energy metabolism.

These results show that the exciting studies in mice about how microbes affect weight gain are also relevant in humans. They are also important because they will allow our group, and other scientists, to investigate how to influence a person's gut microbes - using probiotics and fibre - so they are at a lower risk of developing obesity.

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Gut bacteria play a role in long-term weight gain

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Weight gain happens when we consume more food than we can burn, and weight loss happens when we burn more energy than we consume. But why do some people seem to eat whatever they want and not gain weight, and others appear to gain weight even if they eat reasonable amounts of food?

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For the first time ever, scientists have edited the genetic makeup of viable human embryos - Quartz

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For the first time ever, scientists have edited the genetic makeup of viable human embryos - Quartz

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For the first time ever, scientists have edited the genetic makeup of viable human embryos - Quartz

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Our genetically edited future is nigh. Chinese researchers, who have been at the forefront of experimenting with human embryos using a technology called CRISPR, are...

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Biological Molecules - You Are What You Eat: Crash Course Biology #3

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Archaea: The 'Dark Matter' of the Microbial World - The Atlantic

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Archaea: The 'Dark Matter' of the Microbial World - The Atlantic

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Archaea: The 'Dark Matter' of the Microbial World - The Atlantic

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You've probably heard about your gut bacteria-now get to know your gut archaea.

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The National Academies of Science and Medicine (NASEM) released a report on Feb. 14 exploring the implications of new technologies that can alter the genome of living organisms, including humans.

Although scientists have been able to edit genes for several decades, new genome editing technologies are more efficient, more precise and far less expensive than previous ones. One of these techniques, known as CRISPR-Cas9, could allow for new applications ranging from editing viruses and bacteria to animals, plants and human beings.

For example, scientists could design pest-resistant plants. They could modify the genome of animals, bacteria and viruses to help fight diseases and plagues.

CRISPR could potentially be used by almost anybody willing to tinker with the genome. This, and the fact that it can be used either for beneficial or harmful purposes, have raised fears that CRISPR could become a weapon of mass destruction.

CRISPR could also be used to modify the human genome. The big question scientists are wrestling with is whether these technologies should be used to make modifications in human reproductive cells. Changes made in these cells are heritable from one generation to the next, and are called germline modifications.

Some scientists working with these techniques called for a moratorium for editing that could result in germline modifications. Others thought that a prudent path for using these technologies was needed.

The NASEM report did not endorse a moratorium. But it recommended that at least 10 stringent conditions should be met before authorizing this use. The report also said that more discussion - with wide public participation - was needed before proceeding with human germline modification.

I explore the ethical and policy questions raised by emerging technologies such as CRISPR at the Duke Initiative for Science and Society. I am particularly interested in how different countries regulate these technologies.

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Safe And Ethical Ways To Edit The Human Genome

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The National Academies of Science and Medicine (NASEM) released a report on Feb. 14 exploring the implications of new technologies that can alter the genome of living organisms, including humans. Although scientists have been able to edit genes for several decades, new genome editing technologies are more efficient, more precise and far less expensive than previous ones.

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Gene-editing recently saved the lives of two baby girls who had an incurable form of leukemia. Now, the same type of process has been used to cancel out all the symptoms of a French teenager's sickle cell disease.

Sickle cell disease is one that mainly affects people of African, Caribbean, Middle Eastern, Eastern Mediterranean, and Asian origin. Around 275,000 babies are born with it every single year.

The afflicted have unusually shaped (sickle) blood cells thanks to a coding error in the gene for hemoglobin, the oxygen-carrying segment of red blood cells. This means that the blood cells can't flow effortlessly around the body, and sometimes get trapped in various valves.

The consequences of this life-long condition are complex and varied, but most commonly the patient suffers from bouts of severe anemia due to the inefficient transport of oxygen. They are also at a higher risk of contracting major infections, and can suffer from occasional, extremely painful paroxysms known as sickle cell crises. Stunted growth and strokes are also symptoms in some cases.

Conventional medicine cannot cure it. The only way to potentially cure it to date has been to use bone marrow or stem cell transplants from a healthy donor, which would allow the patient's body to produce healthy blood cells. This does work, but the risk of a dangerous immune response - where the transplanted cells begin attacking the patient's normal cells - is often too high.

However, as reported by a study in the New England Journal of Medicine, a teenager was brought to Necker Children's Hospital in Paris back in 2014 for a game-changing therapy. A specific gene, one that's able to induce an "anti-sickling" effect on red blood cells, was inserted into the patient's own stem cells using a modified virus.

The cells were then allowed to transform into red blood cells, which then began to proliferate around the patient's body. Fifteen months later, the boy, now 15, is not suffering from any of the effects of sickle cell disease. It appears that at least 50 percent of his blood cells have normal hemoglobin and are normally shaped.
Sickle cells in among normal blood cells. Dr Graham Beards/Wikimedia Commons; CC BY-SA 3.0
Although this isn't a cure for the disease, this treatment has proven so effective that the symptoms have been quashed, and he is off all other forms of medication and treatment.

The gene therapy was concocted by scientists at Bluebird Bio based out of Cambridge, Massachusetts. They've treated six other patients with sickle cell disease in the same way, and although the results have yet to be published, it appears that it has not worked as successfully in all of them just yet.

However, trials are still taking place, and the future is looking increasingly bright for those with this unfortunate condition.

[H/T: Associated Press]

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Game-Changing Gene Therapy Nullifies Patient's Sickle Cell Disease

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Gene-editing recently saved the lives of two baby girls who had an incurable form of leukemia. Now, the same type of process has been used to cancel out all the symptoms of a French teenager's sickle cell disease. Sickle cell disease is one that mainly affects people of African, Caribbean, Middle Eastern, Eastern Mediterranean, and Asian origin.

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Understanding the very early stages of embryo development is of interest because this knowledge may help explain why a significant number of human pregnancies fail at this time.

Once a mammalian egg has been fertilised by a sperm, it divides multiple times to generate a small, free-floating ball of stem cells. The particular stem cells that will eventually make the future body, the embryonic stem cells (ESCs) cluster together inside the embryo towards one end: this stage of development is known as the blastocyst. The other two types of stem cell in the blastocyst are the extra-embryonic trophoblast stem cells (TSCs), which will form the placenta, and primitive endoderm stem cells that will form the so-called yolk sac, ensuring that the foetus's organs develop properly and providing essential nutrients.

Previous attempts to grow embryo-like structures using only ESCs have had limited success. This is because early embryo development requires the different types of cell to coordinate closely with each other.

However, in a study published today in the journal Science, Cambridge researchers describe how, using a combination of genetically-modified mouse ESCs and TSCs, together with a 3D scaffold known as an extracellular matrix, they were able to grow a structure capable of assembling itself and whose development and architecture very closely resembled the natural embryo.

"Both the embryonic and extra-embryonic cells start to talk to each other and become organised into a structure that looks like and behaves like an embryo," explains Professor Magdalena Zernicka-Goetz from the Department of Physiology, Development and Neuroscience, who led the research. "It has anatomically correct regions that develop in the right place and at the right time."
Image: Stem cell-modelled embryo at 96 hours (embryonic (magenta) and extra-embryonic (blue) tissue with surrounding extracellular matrix (cyan)). Credit: Berna Sozen, Zernicka-Goetz Lab, University of Cambridge
Professor Zernicka-Goetz and colleagues found a remarkable degree of communication between the two types of stem cell: in a sense, the cells are telling each other where in the embryo to place themselves.

"We knew that interactions between the different types of stem cell are important for development, but the striking thing that our new work illustrates is that this is a real partnership - these cells truly guide each other," she says. "Without this partnership, the correct development of shape and form and the timely activity of key biological mechanisms doesn't take place properly."

Comparing their artificial 'embryo' to a normally-developing embryo, the team was able to show that its development followed the same pattern of development. The stem cells organise themselves, with ESCs at one end and TSCs at the other. A cavity opens then up within each cluster before joining together, eventually to become the large, so-called pro-amniotic cavity in which the embryo will develop.

While this artificial embryo closely resembles the real thing, it is unlikely that it would develop further into a healthy foetus, say the researchers. To do so, it would likely need the third form of stem cell, which would allow the development of the yolk sac, which provides nourishment for the embryo and within which a network of blood vessel develops. In addition, the system has not been optimised for the correct development of the placenta.

Professor Zernicka-Goetz recently developed a technique that allows blastocysts to develop in vitro beyond the implantation stage, enabling researchers to analyse for the first time key stages of human embryo development up to 13 days after fertilisation. She believes that this latest development could help them overcome one of the main barriers to human embryo research: a shortage of embryos. Currently, embryos are developed from eggs donated through IVF clinics.

"We think that it will be possible to mimic a lot of the developmental events occurring before 14 days using human embryonic and extra-embryonic stem cells using a similar approach to our technique using mouse stem cells," she says. "We are very optimistic that this will allow us to study key events of this critical stage of human development without actually having to work on embryos. Knowing how development normally occurs will allow us to understand why it so often goes wrong."

The research was largely funded by the Wellcome Trust and the European Research Council.

Dr Andrew Chisholm, Head of Cellular and Developmental Science at Wellcome, said: "This is an elegant study creating a mouse embryo in culture that gives us a glimpse into the very earliest stages of mammalian development. Professor Zernicka-Goetz's work really shows the importance of basic research in helping us to solve difficult problems for which we don't have enough evidence for yet. In theory, similar approaches could one day be used to explore early human development, shedding light on the role of the maternal environment in birth defects and health."
Reference
Harrison, SE et al.Assembly of embryonic and extra-embryonic stem cells to mimic embryogenesis in vitro. Science; 2 March 2017; DOI: 10.1126/science.aal1810

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european research council (erc) european research council (erc)

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spotlight on stem cells spotlight on stem cells

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animal research school of the biological sciences

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development and neuroscience (pdn) school of the biological sciences

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Scientists create artificial mouse 'embryo' from stem cells for first time

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Understanding the very early stages of embryo development is of interest because this knowledge may help explain why a significant number of human pregnancies fail at this time. Once a mammalian egg has been fertilised by a sperm, it divides multiple times to generate a small, free-floating ball of stem cells.

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Scientists have discovered what they say could be fossils of some of the earliest living organisms on Earth.

They are represented by tiny filaments, knobs and tubes in Canadian rocks dated to be up to 4.28 billion years old.

That is a time not long after the planet's formation and hundreds of millions of years before what is currently accepted as evidence for the most ancient life yet found on Earth.

The researchers report their investigation in the journal Nature.

As with all such claims about ancient life, the study is contentious. But the team believes it can answer any doubts.

The scientists' putative microbes from Quebec are one-tenth the width of a human hair and contain significant quantities of haematite - a form of iron oxide or "rust".

Matthew Dodd, who analysed the structures at University College London, UK, claimed the discovery would shed new light on the origins of life.

"This discovery answers the biggest questions mankind has asked itself - which are: where do we come from and why we are here?

"It is very humbling to have the oldest known lifeforms in your hands and being able to look at them and analyse them," he told BBC News.

The fossil structures were encased in quartz layers in the so-called Nuvvuagittuq Supracrustal Belt (NSB).

The NSB is a chunk of ancient ocean floor. It contains some of the oldest volcanic and sedimentary rocks known to science.

The team looked at sections of rock that were likely laid down in a system of hydrothermal vents - fissures on the seabed from which heated, mineral-rich waters spew up from below.

Today, such vents are known to be important habitats for microbes. And Dr Dominic Papineau, also from UCL, who discovered the fossils in Quebec, thinks this kind of setting was very probably also the cradle for lifeforms between 3.77 and 4.28 billion years ago (the upper and lower age estimates for the NSB rocks).

He described how he felt when he realised the significance of the material on which he was working: "I thought to myself 'we've got it, we've got the oldest fossils on the planet'.

"It relates to our origins. For intelligent life to evolve to a level of consciousness, to a point where it traces back its history to understand its own origin - that's inspirational."

Any claim for the earliest life on Earth attracts scepticism. That is understandable. It is often hard to prove that certain structures could not also have been produced by non-biological processes.

In addition, analysis is complicated because the rocks in question have often undergone alteration.

The NSB, for example, has been squeezed and heated through geological time

At present, perhaps the oldest acknowledged evidence of life on the planet is found in 3.48-billion-year-old rocks in Western Australia.

This material is said to show remnants of stromatolites - mounds of sediment formed of mineral grains glued together by ancient bacteria.

An even older claim for stromatolite traces was made in August last year. The team behind that finding said their fossil evidence was 3.70 billion years old.

Nonetheless, the UCL researchers and their colleagues say they have worked extremely hard to demonstrate the greater antiquity for their structures.

Dr Papineau does concede though that the idea of metabolising micro-organisms using oxygen so soon after the Earth's formation will surprise many geologists.

"They would not consider that there were organisms breathing oxygen at this time. It brings back the production of oxygen on the Earth's surface, albeit by tiny amounts, to the beginning of the sedimentary record," he said.

Prof Nicola McLoughlin from Rhodes University, South Africa, was not connected with the research.

She commended the scholarship but felt the data presented by the UCL-led team fell short.

"The morphology of these argued iron-oxidising filaments from Northern Canada is not convincing," she told BBC News.

"In recent deposits we see spectacular twisted stalks, often arranged in layers, but in the highly metamorphosed rocks of the Nuvvuagittuq belt the filaments are much simpler in shape.

"The associated textural and geochemical evidence of graphite in carbonate rosettes and magnetite-haematite granules is careful work, but provides only suggestive evidence for microbial activity; it does not strengthen the case for the biogenicity of the filaments."

She also said the maximum age of the rocks had proven to be very controversial, and that the true age was more likely to be closer to the 3.77-billion-year age.

Part of the interest in ancient life is in the implication it has for organisms elsewhere in the Solar System.

"These (NTB) organisms come from a time when we believe Mars had liquid water on its surface and a similar atmosphere to Earth at that time," said Mr Dodd.

"So, if we have lifeforms originating and evolving on Earth at this time then we may very well have had life beginning on Mars."

If that is the case then, according to Dr Papineau, recent Nasa rover missions to the Martian surface may have been looking for signs of life in the wrong places.

He said that the Mars Exploration Rovers (MER), Spirit and Opportunity, and the more recent Curiosity robot mission had overlooked areas that might have had rocks produced by hydrothermal vents.

"On the surface of Mars there have been missed opportunities. The MER Opportunity in 2003 found promising formations but there was no analysis. And the Spirit rover went straight past another near the Comanche outcrop in Gusev crater."

The suggestion that life had already arisen "just" a few hundred million years after the Earth had formed is intriguing in light of debates about whether life on Earth was a rare accident or whether biology is a common outcome given the right conditions.

Follow Pallab on Twitter.

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Earliest evidence of life on Earth 'found'

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Scientists have discovered what they say could be fossils of some of the earliest living organisms on Earth. They are represented by tiny filaments, knobs and tubes in Canadian rocks dated to be up to 4.28 billion years old.

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Scientists at the University of Ottawa have developed a way of growing human cells and tissue on apples.

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http://www.bbc.co.uk/news/science-environment-39142941

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The last woolly mammoths to walk the Earth were so wracked with genetic disease that they lost their sense of smell, shunned company, and had a strange shiny coat.

That's the verdict of scientists who have analysed ancient DNA of the extinct animals for mutations.

The studies suggest the last mammoths died out after their DNA became riddled with errors.

The knowledge could inform conservation efforts for living animals.

There are fewer than 100 Asiatic cheetahs left in the wild, while the remaining mountain gorilla population is estimated at about 300. The numbers are similar to those of the last woolly mammoths living on Wrangel Island in the Arctic Ocean around 4,000 years ago.

Dr Rebekah Rogers of the University of California, Berkeley, who led the research, said the mammoths' genomes "were falling apart right before they went extinct".

This, she said, was the first case of "genomic meltdown" in a single species.

"You had this last refuge of mammoths after everything has gone extinct on the mainland," she added.

"The mathematical theories that have been developed said that they should accumulate bad mutations because natural selection should become very inefficient."

The researchers analysed genetic mutations found in the ancient DNA of a mammoth from 4,000 years ago. They used the DNA of a mammoth that lived about 45,000 years ago, when populations were much larger, as a comparison.

Woolly mammoths were once common in North America and Siberia. They were driven to extinction by environmental factors and possibly human hunting about 10,000 years ago. Small island populations clung on until about 4,000 years ago.

"There was this huge excess of what looked like bad mutations in the genome of the mammoth from this island," said Dr Rogers.

"We found these bad mutations were accumulating in the mammoth genome right before they went extinct."

Knowledge of the last days of the mammoth could help modern species on the brink of extinction, such as the panda, mountain gorilla and Indian elephant. The lesson from the woolly mammoth is that once numbers drop below a certain level, the population's genetic health may be beyond saving. Genetic testing could be one way to assess whether levels of genetic diversity in a species are enough to give it a chance of survival. A better option is to stop numbers falling too low.

"When you have these small populations for an extended period of time they can go into genomic meltdown, just like what we saw in the mammoth," said Dr Rogers.

"So if you can prevent these organisms ever being threatened or endangered then that will do a lot more to help prevent this type of genomic meltdown compared to if you have a small population and then bring it back up to larger numbers because it will still bear those signatures of this genomic meltdown."

Scientists think the genetic mutations may have given the last woolly mammoths "silky, shiny satin fur". Mutations may have also led to a loss of olfactory receptors, responsible for the sense of smell, as well as substances in urine involved in social status and attracting a mate.

Love Dalen is professor of evolutionary genetics at the Swedish Museum of Natural History and head of the team of scientists that originally published the DNA sequences of the mammoths.

He said they found "many deletions, big chunks of the genome that are missing, some of which even affected functional genes".

"This is a very novel result," he said. "If this holds up when more mammoth genomes, as well as genomes from other species, are analysed, it will have very important implications for conservation biology."

The research is published in the journal, PLOS Genetics.

Follow Helen on Twitter.

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DNA clues to why woolly mammoth died out

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The last woolly mammoths to walk the Earth were so wracked with genetic disease that they lost their sense of smell, shunned company, and had a strange shiny coat. That's the verdict of scientists who have analysed ancient DNA of the extinct animals for mutations.

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Update: CRISPR

(Photo Credit: NIH/NIAID/Flickr)

It's been almost two years since we learned about CRISPR, a ninja-assassin-meets-DNA-editing-tool that has been billed as one of the most powerful, and potentially controversial, technologies ever discovered by scientists. In this episode, we catch up on what's been happening (it's a lot), and learn about CRISPR's potential to not only change human evolution, but every organism on the entire planet.

Out drinking with a few biologists, Jad finds out about something called CRISPR. No, it's not a robot or the latest dating app, it's a method for genetic manipulation that is rewriting the way we change DNA. Scientists say they'll someday be able to use CRISPR to fight cancer and maybe even bring animals back from the dead. Or, pretty much do whatever you want. Jad and Robert delve into how CRISPR does what it does, and consider whether we should be worried about a future full of flying pigs, or the simple fact that scientists have now used CRISPR to tweak the genes of human embryos.
This episode was reported and produced by Molly Webster and Soren Wheeler. Special thanks to Jacob S. Sherkow.
Support Radiolab by becoming a member today at Radiolab.org/donate.

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Update: CRISPR (Photo Credit: NIH/NIAID/Flickr) It's been almost two years since we learned about CRISPR, a ninja-assassin-meets-DNA-editing-tool that has been billed as one of the most powerful, and potentially controversial, technologies ever discovered by scientists.

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New Link Found Between Sex and Viruses - Science & Technology Research News

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New Link Found Between Sex and Viruses - Science & Technology Research News

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New Link Found Between Sex and Viruses - Science & Technology Research News

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Sexual reproduction and viral infections have a lot in common. According to new research, both processes rely on a single protein for the seamless fusion of two cells-sperm and egg cells and virus and cell membrane. This protein is widespread among viruses, single-celled protozoans, and many plants and arthropods, but is not found in fungi...

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The smallest Cas9 genetic scissors (so far) - Science Magazine

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The smallest Cas9 genetic scissors (so far) - Science Magazine

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The smallest Cas9 genetic scissors (so far) - Science Magazine

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Credit: IBS Scientists at the Center for Genome Engineering, within the Institute for Basic Science (IBS), in collaboration with KIM Eunji (ToolGen Inc.) and KIM Jeong Hun (Seoul National Universit..

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Roads are driving rapid evolutionary change in our environment - Knowridge

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Roads are driving rapid evolutionary change in our environment - Knowridge

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Roads are driving rapid evolutionary change in our environment | Knowridge Science Report - Knowridge

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Roads are causing rapid evolutionary change in wild populations of plants and animals according to a Concepts and Questions paper published in Frontiers in Ecology and the Environment. The paper is available now online in 'early view' ahead of being featured on the cover in the print edition on March 1.

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Why blue whales are so enormous - BBC Earth

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Why blue whales are so enormous - BBC Earth

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How Crossbills and Other Birds Are Rewriting the Rules of Evolution - Audubon

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How Crossbills and Other Birds Are Rewriting the Rules of Evolution - Audubon

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What's The Science Of Superbugs? - Medical Daily

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What's The Science Of Superbugs? - Medical Daily

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What's The Science Of Superbugs? - Medical Daily

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Antibiotic resistance bacteria aren't as dangerous as you may have heard -- yet. What you need to know.

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Impact of climate change on mammals and birds 'greatly under-estimated' - Science Magazine

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Impact of climate change on mammals and birds 'greatly under-estimated' - Science Magazine

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Impact of climate change on mammals and birds 'greatly under-estimated' - Science Magazine

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Credit: Liana Joseph An international study published today involving University of Queensland research has found large numbers of threatened species have already been impacted by climate change. ..

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Bondage, Cannibalism, and Castration—Spiders' Wild Sex Lives - National Geographic

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Bondage, Cannibalism, and Castration—Spiders' Wild Sex Lives - National Geographic

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Bondage, Cannibalism, and Castration-Spiders' Wild Sex Lives - National Geographic

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As love fills the air this Valentine's Day, National Geographic takes a look at the animal kingdom's most inventive sweethearts.

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How the Endangered Species Act Helps Save Humans, Too - TIME

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How the Endangered Species Act Helps Save Humans, Too - TIME

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How the Endangered Species Act Helps Save Humans, Too - TIME

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Republicans are trying to reform the law

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ANTibiotic: Bacteria from African ant used to create MRSA-killing drug - International Business Times, UK Edition

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ANTibiotic: Bacteria from African ant used to create MRSA-killing drug - International Business Times, UK Edition

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ANTibiotic: Bacteria from African ant used to create MRSA-killing drug - International Business Times, UK Edition

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African fungus-growing plant-ant used to produce new antibiotic that is potent against superbugs.

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How many of them are vaccinated? Henrik Winther Andersen/Shutterstock

The measles outbreak traced back to Disneyland has spread to eight states, with as many as 95 cases reported by January 28. Media outlets are highlighting the rise of anti-vaccination sentiments. Scientists are expressing their dismay at people who reject sound medical advice and put their families and communities in harm's way.

Measles was considered eliminated in the United States in 2000. But if the first month of 2015 is any indication, this year will easily beat the record number of measles cases recorded in 2014.

The narrative during this outbreak, or any measles outbreak really, is that measles is a highly transmissible disease. So transmissible in fact that 90- 95% of people must be vaccinated in order to protect the entire population, or achieve what is called herd immunity.

That is partly true. Measles is highly transmissible, not least because people can be contagious days before symptoms develop. But there are three problems with this line of reasoning about vaccination rates.

First, the numbers are based on calculations that assume a world of random mixing. Second, the vaccination coverage is not a perfect measure of immunity in the population. Third, and most problematic in my view, it gives people a seemingly scientific justification for not getting vaccinated - after all, if not everyone needs to get vaccinated in order to attain herd immunity, can it really be so bad if I opt out of it?

Zebras by Andrzej Kubik/Shutterstock

What exactly is herd immunity?

Let's look at the concept of herd immunity first. The basic idea is that a group (the "herd") can avoid exposure to a disease by ensuring that enough people are immune so that no sustained chains of transmission can be established. This protects an entire population, especially those who are too young or too sick to be vaccinated. But how many people need to be immune to achieve this?

In order to calculate the number of people who need to be immune for herd immunity to be effective, we need to know how many people will get infected, on average, by an infectious person.

Imagine that a newly infected person will on average pass on the disease to two other people. Those two will each infect another two people, who will themselves pass it on, and so on, resulting in the classical pattern of an exponentially growing outbreak.

Marcel Salathé, Author provided

In order to stop the growth in the number of transmissions, we need to ensure that each individual case causes, on average, less than one new infection. So, let's say that one case leads on average to two more infections, but instead we want that number to be less than one. That means at least 50% of the population needs to be immune, so that at most, only one of the two people who might have been infected by an individual will be.

Marcel Salathé

How many people need to get vaccinated to achieve herd immunity?

So, how do we calculate what fraction of a population needs to be immune to reach herd immunity? First, we need to know what the reproduction number, or R, is. That's how many new cases a single case of an infection will cause.

Imagine that you are infected in a completely susceptible population, and you pass on the infection to five other people (ie R=5). In order to prevent an outbreak, at least four out of those five people, or 80% of the population in general, should be immune. Put differently, 20% of the population may remain individually susceptible, but the population would still remain protected.

So if you can estimate the reproduction number for a given disease, you can calculate the fraction of the population that needs to be immune in order to attain herd immunity.

For influenza and Ebola, the number R is about two. For polio and smallpox, it is around five to eight. But for measles it is much higher, somewhere between 10 and 20. And because of that, the goal for measles vaccination coverage is typically around 90-95% of a population.

But there's a problem with this calculation.

The population is not random

The assumption underlying the calculation for herd immunity is that people are mixing randomly, and that vaccination is distributed equally among the population. But that is not true. As the Disneyland measles outbreak has demonstrated, there are communities whose members are much more likely to refuse vaccination than others.

Geographically, vaccination coverage is highly variable on the level of states, counties, and even schools. We're fairly certain that opinions and sentiments about vaccination can spread in communities, which may in turn lead to polarized communities with respect to vaccination.

And media messages, especially from social media, may make the problem worse. When we analyzed data from Twitter about sentiments on the influenza H1N1 vaccine during the swine flu pandemic in 2009, we found that negative sentiments were more contagious than positive sentiments, and that positive messages may even have back-fired, triggering more negative responses.

And in measles outbreak after measles outbreak, we find that the vast majority of cases occurred in communities that had vaccination coverages that were way below average.

The sad truth is this: as long as there are communities that harbor strong negative views about vaccination, there will be outbreaks of vaccine-preventable diseases in those communities. These outbreaks will happen even if the population as a whole has achieved the vaccination coverage considered sufficient for herd immunity.

Marcel Salathé

If negative vaccination sentiments become more popular in the rest of the population as well, we may start to see more sustained transmission chains. Once those chains are sufficiently frequent to connect under-vaccinated communities, we may again be in a situation of endemic measles.

The solution often proposed is that we should do a better job of convincing people that vaccines are safe. I'm all for it. But I would also suggest that we should stop basing our vaccination policies on models that made sense in a world of constrained vaccine supply, and aim for 100% vaccination coverage among those who can get vaccinated.

This would also solve another problem, often glanced over: There are many people who cannot get vaccinated for medical reasons, either because they are too young, or because they have other conditions that prevent them from acquiring immunity through vaccination.

Herd immunity against measles requires that 90-95% of the entire population are immune, whereas vaccination coverage is measured as the percentage vaccinated of the target population - which only includes people who are eligible for vaccination. This means that to achieve 95% immunity in the population for measles, vaccination coverage needs to be higher than 95%. This is the scientific argument for a public health policy that aims at 100% vaccination coverage.

More importantly, there is an ethical argument to be made for the goal of 100% vaccination coverage. It sends the right message. Everyone who can get vaccinated, should get vaccinated - not only to protect themselves, but to protect those who can't, through herd immunity.

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Herd immunity and measles: why we should aim for 100% vaccination coverage

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The measles outbreak traced back to Disneyland has spread to eight states, with as many as 95 cases reported by January 28. Media outlets are highlighting the rise of anti-vaccination sentiments. Scientists are expressing their dismay at people who reject sound medical advice and put their families and communities in harm's way.

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Between Greenland and Norway in the mid-Atlantic ocean, 7,546ft (2300m) below the surface, there is a black and smoky region where hot water spouts up from the sea bed. This strange place is called "Loki's castle" after the shape-shifting Norse God Loki: the one Tom Hiddleston played in The Avengers.

Close to Loki's castle, there lives a microbe like no other on Earth.

In 2015, a team of scientists led by microbiologist Thijs Ettema of Uppsala University in Sweden reported that they had discovered a new kind of micro-organism. They found genetic traces of this single-celled microbe in sea-floor sediments 9 miles (15km) from Loki's castle.

Writing in the journal Nature, the team called the new microbe " Lokiarchaeota". This quickly got shortened to "Loki".

This mysterious microbe turned out to be the closest living relative of the eukaryotes, the group that includes all complex living organisms; from plants and fungi to insects and humans. That means Loki could help us understand how the eukaryotes first came into being. In other words, Loki may help explain why people - and all other complex life - exist.

Loki the god has been described as "a staggeringly complex, confusing, and ambivalent figure". The same is true of eukaryotes. How eukaryotes first evolved is a puzzle that continues to flummox scientists the world over.

If the eukaryotes had never formed, neither would we

Until a few decades ago, biologists thought that there were essentially two kinds of life on this planet: eukaryotes and prokaryotes. While the eukaryotes include both single-celled organisms and more complex ones like mushrooms and chimpanzees, the prokaryotes are all single-celled. The most famous prokaryotes are the bacteria.

The key difference between prokaryotes and eukaryotes is the complexity of the cells. Prokaryotes are simple cells, with only a few internal structures, whereas the cells of eukaryotes are much more intricate. Eukaryotic cells also tend to be bigger, often ten times as large as prokaryotic cells.

It is the complexity of eukaryotic cells, and the resulting extra abilities, that allow them to bolt together to form multicellular organisms like us. Prokaryotes cannot do this. So if the eukaryotes had never formed, neither would we.

This straightforward split between simple and complex held sway for decades, until one scientist showed that there was more to it.

In the late 1960s, American microbiologist Carl Woese decided to look at organisms' DNA sequences to figure out how they were all related.

Woese identified a gene that all organisms carry, and compared all the different versions of it. Species that had more similar versions of the gene were probably closely related. In this way he built up a family tree of all the known living organisms.

Instead of two domains of life, there were three

Woese's analysis revealed that there were two kinds of prokaryote. As well as the bacteria, there was an entirely new group that he called "archaea".

Like the bacteria, the archaea were single-celled organisms with relatively simple cells. On the outside they looked similar to bacteria, but genetically they were clearly distinct. Archaea are found all over the world, and many of them can grow in extreme conditions such as near-boiling water.

Woese had redrawn the tree of life. Instead of two domains of life, there were three: bacteria, archaea and eukaryotes. In 1977, he published his findings in the journal . They were so revolutionary, Woese made the front page of the New York Times.

Woese's ideas would also set the stage for scientists to explain how the eukaryotes were born.

The eukaryotes are the youngest of the three domains. While bacteria and archaea may date back over 3 billion years, the eukaryotes probably only came into existence around 2 billion years ago.

But how and why did this happen? Did the eukaryotes arise from the archaea, or from the bacteria? And why did eukaryotic cells become so big and complex, while the others stayed tiny?

The first eukaryote must have formed when a host cell swallowed a bacterium

Perhaps the biggest clue comes from tiny structures inside eukaryotic cells called "mitochondria". These sausage-shaped objects are the cells' source of power, and without them eukaryotic cells could not grow as large as they do.

A decade before Woese published his tree of life, the biologist Lynn Margulis had begun arguing that mitochondria are descended from bacteria. Somehow these bacteria ended up inside another, larger cell, where they gradually became mitochondria. In 1978, the year after Woese's study, Margulis's idea was confirmed by experiment.

This means that the first eukaryote must have formed when a host cell swallowed a bacterium. Once that had happened, the two established a long-lasting and mutually-beneficial relationship, and the eukaryotes were on their way.

But that raises an obvious question. What was the host cell? Was it another bacterium, or an archaean?

The simplest way to approach this question is to take a leaf out of Woese's book, and look at eukaryotes' genes. Are they more similar to those of archaea, or those of bacteria? That would give a hint about which group they are descended from.

It's the first prokaryote which has eukaryote building blocks

This question is trickier to answer than you might expect. The typical eukaryotic genome contains a mix of bacterial and archaeal genes, as well as genes specific to eukaryotes.

However, by 2010 it was pretty clear that the host cell was an archaean.

But there was still a problem. No known archaean seemed to be equipped to be a host cell. They all lacked the genetic and cellular machinery necessary to play host to another cell.

"The discovery of Loki changed that," says Ettema.

When Loki was found in 2015, it was immediately apparent that it was an archaean. But it was an archaean that had some surprising similarities to eukaryotes.

"It's the first prokaryote which has eukaryote building blocks," says Ettema. "We found a battery of 100 genes specifically related to eukaryotes."

All that Ettema's team found in the sea bed were fragments of Loki's genes. They have never actually seen Loki itself

In particular, Loki's genome carries the genes for proteins called small GTPases. These are important for the shape and movement of cells. For example, eukaryotic cells have "skeletons" that maintain their shape, and the small GTPases control the skeleton. They also regulate sets of proteins that allow membranes to bend.

The fact that Loki has these genes suggests that, like a eukaryote, it has an internal skeleton - and that it could bend its outer membrane to engulf a bacterium. That makes it a suitable host cell, or at least the closest thing we know to one.

It may be that Loki belongs to a group of archaea that almost managed to become eukaryotes, but never quite made it. Ettema jokingly calls it "a failed eukaryote".

It looks like a convincing story. But there is one big problem.

All that Ettema's team found in the sea bed were fragments of Loki's genes. They have never actually seen Loki itself, let alone cultured it in their lab.

Ettema jokingly calls it "a failed eukaryote"

So we do not know if Loki's small GTPases perform the same functions as they do in eukaryotes. The only way to find out is to study living Loki cells.

That will be difficult, even if someone manages to find some Loki cells. These microbes live in the deep sea, where nutrients are scarce and microbes grow only slowly.

Still, Ettema and his colleagues have not given up looking for Loki. As well as the deep sea, it also seems to live in shallow sediments, estuaries and hot springs.

Meanwhile, other scientists are drawing on the evidence from Loki to refine our ideas about the origin of eukaryotes.

After the discovery of Loki, cell biologist Buzz Baum of University College London in the UK and his team made some suggestions about how the first eukaryotes could have evolved from simpler archaea. In a paper published in June 2016 in Trends in Cell Biology, they studied the eukaryote-like genes found in the Loki genome, especially the small GTPases.

The more likely possibility is that archaea and bacteria first formed a stable partnership

In eukaryotes, GTPase proteins are involved in shuttling material across membranes inside the cell. To help with this, each GTPase carries "lipids": small fat molecules that help anchor it to the membranes. Without these lipid anchors, the GTPases would not be able to do their jobs.

The Loki genome does not have the necessary tools to add lipids to GTPase proteins. This implies that, if Loki really does show us what the ancestor of eukaryotes was like, the ancestor could not use its GTPases in this way. It would have needed to acquire the ability somehow.

Bacteria do carry plausible precursors of the lipid-adding machinery. This implies that an archaean somehow picked up the lipid modification enzymes from bacteria.

Baum argues that this cannot have happened suddenly. If an archaean were to suddenly pick up so many new genes, its cellular processes would have been disrupted and it would probably have died.

The linking of the two cells was anything but sudden

The more likely possibility is that archaea and bacteria first formed a stable partnership, and then gradually transferred genetic material and lipids a bit at a time. This sustained partnership could have led to the development of internal compartments and membrane trafficking.

In other words, the genesis of eukaryotes was a slow process. The dramatic "swallowing" of a bacterium, while it probably did happen, was only one step of many.

Baum also has a neat idea about how the swallowing happened.

The classic image is an "outside-in" process, in which the archaeal host engulfed and "ate" the bacterium - but for some reason did not digest it. It is hard to see how this could have worked: if the archaean was eating a piece of food, why would it not digest it?

Ettema has found new relatives of Loki that are also closely related to eukaryotes

So in 2014, Baum and his colleague David Baum proposed an alternative that he calls the "inside-out" model. Again, this is built on the assumption that the linking of the two cells was anything but sudden.

Baum suggests that the archaeal host first extended protrusions towards the bacteria in its environment. These protrusions were not an attempt to eat the bacteria: instead, they allowed the transfer of materials between the two cells.

Eventually, the archaean formed more and more of these protrusions until they completely enveloped the bacterium. "These protrusions from a single cell then fused with each other to form a continuous outer layer," says Baum's post-doctoral fellow Gautam Dey.

For now we cannot tell if Baum's ideas are correct. But if Ettema can find more of Loki's relatives, we might get enough information to make a firm judgement.

In the last few months, Ettema has found new relatives of Loki that are also closely related to eukaryotes. The work is still in the early stages, but he says these other archaea also possess some of the building blocks of eukaryotes.

For now we cannot tell if Baum's ideas are correct

We do not yet know what these strange microorganisms will teach us about the origin of eukaryotes.

Ettema says the puzzle is still being put together piecemeal. When Loki or something similar is finally isolated, we should be able to find out how it makes a living and what it uses its eukaryote-like proteins for.

And that, in turn, will tell us about the microorganism that ultimately gave birth to all of us.
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A microbe no one has even seen could explain our origins

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Between Greenland and Norway in the mid-Atlantic ocean, 7,546ft (2300m) below the surface, there is a black and smoky region where hot water spouts up from the sea bed. This strange place is called "Loki's castle" after the shape-shifting Norse God Loki: the one Tom Hiddleston played in The Avengers .

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Tuck your napkin under your chin. We’re about to serve up a tale of love, loss, and lamb chops.

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“A forest is much more than what you see,” says ecologist Suzanne Simard. Her 30 years of research in Canadian forests have led to an astounding discovery -- trees talk, often and over vast distances. Learn more about the harmonious yet complicated social lives of trees and prepare to see the natural world with new eyes.

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Can genetic testing help improve performance?

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Can genetic testing help improve performance?

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enetic analysis companies are forging alliances with personal trainers, chiropractors, and coaches around the world to market genomics tests that they say can help athletes at all levels tailor their workouts to their DNA.

They have struck deals with the Baylor University football team in Texas, with soccer teams in the English Premier League and in Egypt, and with an elite training facility in Arizona for top track and field athletes, including several who competed in the Rio Games.

Yet there is little science to back up the claims that a genetic analysis could identify if a particular athlete is, say, predisposed to benefit from a certain type of exercise, prone to tendon injuries, or wired to have trouble recovering from tough workouts.

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Such tests "have no role to play in talent identification or the individualised prescription of training to maximise performance," according to a consensus statement published last year in the British Journal of Sports Medicine, signed by two dozen experts in genomics and sports performance.

Or as Harvard geneticist Dr. Robert Green puts it: "The notion that they're somehow tailoring these recommendations on the basis of your DNA is nonsense."

That hasn't stopped such claims from proliferating. The number of companies selling fitness-oriented consumer genetic tests grew to at least 39 last year, nearly double the market size in 2013. They're part of a booming industry of lifestyle-oriented consumer genetic tests, which purport to use your DNA to tell you everything from how to eat to which supplements to take to what kind of wine you'll like.

Companies marketing these tests, which generally cost a few hundred dollars, say they're aware of the field's limitations.

"We deliberately under-claim everything. We do not want to overstate what genetics can do," said Andrew Steele, product head for UK-based DNAFit - and a bronze medalist in track in the 2008 Beijing Games.

How coaches use the information is up to them, "because there's no data to say that you should use them in one way or another," said Dr. Paul Billings, the chief medical officer of Berkeley, Calif.-based Kinetic Diagnostics, which until recently sold a $400 genetic test for athletes but has stopped taking orders as it refines its business model.

Marketing in gyms and an NFL stadium

Despite the limitations of genetic analysis, other companies are still pushing these tests as powerful tools that can give athletes a winning edge.

Recreational athletes are one key market: "The lowest hanging fruit ... are the millions of people who are trying to do something" about their weight or fitness, said Kurt Johnsen, CEO of Texas-based Simplified Genetics, which sells "Simply Fit" tests for $249 and $499.

Companies are also moving full-speed ahead in courting coaches and personal trainers.

Johnsen, a former yoga instructor, said his company is negotiating a deal with a chain of fitness clubs that would add the Simply Fit test to a premium gym membership. He wouldn't name the gym, but he said it's a national chain.

"Is your workout working?" asks a Simply Fit brochure, which Johnsen said he uses to present the test to potential customers in the fitness world. The brochure promises that once the test has "provided you with the most accurate information for your genotype, you will be able to reach your fitness goals with our thorough reports of what to DO, EAT and TAKE."

Athletigen, meanwhile, is in the planning stages of a partnership with Baylor football that would use players' genetic data to design personalized training programs. The company touts its use of "cutting edge sports science" to help athletes "reach their highest levels of performance." (Baylor didn't respond to repeated requests for comment.)

Meanwhile, Orig3n, a Boston-based biotech with a side business selling consumer genetic tests, is using the cachet of a top NFL team to market its services. An Orig3n booth inside Levi's Stadium, where the San Francisco 49ers play, collects blood from fans for medical research - and sells a $149 do-it-yourself genetic test kit that promises to give you "unprecedented insights about your fitness potential."

To sweeten the deal, you'll also get entered into a contest to win a signed 49ers football, helmet, or jersey.

Brent Schoeb, the team's vice president of corporate partnerships, didn't respond to questions about the science behind the genetic tests, except to say that "our goal is to ensure that Orig3n generates positive brand awareness through the relationship."

Notably not participating in all the genotyping: 49ers players themselves.

It's time to get hyped for this weekend's #SFvsCAR. Go Niners! #FaithfulDNA https://t.co/Z7M9gqDPWN pic.twitter.com/mS7gN9V1kK

- ORIG3N Inc (@ORIG3N_Inc) September 16, 2016

Gathering evidence to back up advice

As proof that they're on to something, the testing companies point to a small but growing body of scientific literature exploring how genetic differences contribute to individual strength, flexibility, speed, and propensity for injuries. And some companies say they're steadily gathering additional evidence to back up their advice.

Consider a study supported by DNAFit and published earlier this year. Researchers performed genetic analysis on 28 athletes from different sports and then randomly assigned them to either a high- or low-intensity training program.

Half the group was assigned to the training style that DNAFit's algorithm recommended for them based on their genes; the other half was assigned to the training style deemed inappropriate.

After eight weeks, the "matched" group performed better on measures of explosive power and aerobic fitness than the "mismatched" group. (The athletes didn't know which group they were in; nor did those evaluating their fitness.) Similar results were seen in another study on 39 soccer players, reported in the same paper.

One caveat: Such studies are often small and in homogenous populations. The study on DNAFit, for instance, looked at just male college students at a university in northern England.

And there's concern among academic researchers that genetic test companies tend to cite studies "inappropriately," using "selective quotations or taking little bit of information and extrapolating way beyond what we say," said Alun Williams, a geneticist who studies sports and exercise at Britain's Manchester Metropolitan University and coauthored the 2015 consensus statement.

Yet another problem, experts say: Associations observed in large studies of thousands of people don't necessarily translate into useful advice for individuals.

Harvard's Green illustrates the flaw this way: Imagine that you have thousands of people. Half of them have a genetic variant linked to sprinting speed; they get green jerseys. The other half have a genetic variant associated with no advantage in sprinting; they get red jerseys.

Line them up side by side, blow your whistle, and send them off on a short foot race. On average, the runners with the "speed" marker will probably finish a few steps ahead of the runners without it. But the race will be a big blur of color, reds and greens mixed together, undetectable to the eye who's faster.

"It's the difference between a population finding where with enough people you do see a statistically significant difference, and the ability to turn around and use that as a predictive tool in an individual person," said Green, who also practices at Brigham and Women's Hospital in Boston.

Spent the day today at @ALTISworld onboarding world leaders in athletic performance to Iris! #CarryTheShield https://t.co/1o8zVat3VF pic.twitter.com/sjKg913VWR

- Athletigen (@Athletigen) October 25, 2016

Tailoring workouts to a genetic readout

Despite the shaky science, the promise of harnessing genetics info is tantalizing enough that some athletes and coaches are jumping in.

ALTIS, an Arizona training facility, has worked with Canada-based testing company Athletigen in recent years to genotype elite track and field athletes. Just last week, some of the athletes got set up with a smartphone app. It includes a dashboard where they can pull up Athletigen's interpretation of their genetic data, which might include "high sensitivity to caffeine," "normal sensitivity to saturated fats," and "normal daily calorie intake."

In a demo on Athletigen's website, coaches get a version that lets them hone in on each athlete's data. (Sample updates might include the fact that training load has been "trending up" over the past two weeks).

Athletigen CEO Jeremy Koenig emphasizes that his company isn't making recommendations on how to use the data.

That's up to coaches like Dan Pfaff.

Pfaff, the ALTIS head coach, said when he designs training regimens for some athletes, he considers whether they have genetic variants associated with more difficult recovery from exercise. If so, they might get more days off or shorter workout sessions. Or they might move practice from the track to the more forgiving grass.

How about those who might be genetically predisposed to tendon injuries? They may get a more intense daily orthopedic exam.

Pfaff speaks cautiously about the promise of genetic testing for athletes. He insists that he and other ALTIS coaches never use genetic testing to identify talent. They never make decisions based on a single genetic marker, instead pooling together, say, seven to 10 genetic markers to decide if an athlete is predisposed to have trouble recovering from exercise.

Pfaff bristles when people uniformly dismiss all companies in the space as "charlatans and snake oil salesmen," he said. But he acknowledges it's too early to say for sure if the Athletigen tests have helped his athletes.

Some athletes who have tried it have no such hesitation.

British long jumper Greg Rutherford was quoted in a press release this past spring saying that acting on the results of his DNAFit test was helping him hit "huge personal bests in the weight room."

Rutherford went on to win a bronze medal in this past summer's Rio Olympics. He's now a paid spokesperson for DNAFit.

About the Author

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How genetic testing of questionable value is infiltrating the world of sports

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enetic analysis companies are forging alliances with personal trainers, chiropractors, and coaches around the world to market genomics tests that they say can help athletes at all levels tailor their workouts to their DNA.

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Mosquito army released in Zika fight in Brazil & Colombia

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Mosquito army released in Zika fight in Brazil & Colombia

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Scientists are planning to release an army of millions of modified mosquitoes in areas of Brazil and Colombia.

They say the unusual approach is an attempt to provide "revolutionary protection" against mosquito-borne diseases such as Zika and chikungunya.

The mosquitoes are infected with a bug called Wolbachia which reduces their ability to spread viruses to people.

The $18m dollar project is funded by an international team of donors, including the Bill and Melinda Gates Foundation.

"Vaccinating mosquitoes"

The scheme - which aims to start in early 2017 - is also financed by local governments in Latin America, the US and the UK.

Wolbachia is a naturally occurring bacterium that infects 60% of insect species worldwide, but scientists say it does not harm humans.

The bug does not usually infect the Aedes aegypti mosquito - the species mostly responsible for spreading a host of diseases such as Zika, dengue fever and cikungunya.

But over the last decade researchers working for the Eliminate Dengue Program have found a way to inject the bug into Aedes mosquitoes.

And researchers say small-scale observational trials in Brazil, Colombia, Australia, Indonesia and Vietnam have shown that once released, the modified mosquitoes can cut the spread of dengue to humans.

It has been shown to do the same for Zika and chikungunya in laboratory-based tests.

Dr Trevor Mundel, of the Bill and Melinda Gates Foundation, said: "Wolbachia could be a revolutionary protection against mosquito-borne disease.

"It's affordable, sustainable, and appears to provide protection against Zika, dengue and a host of other viruses.

"We are eager to study its impact and how it can help countries."

Researchers now plan to expand the trials to large urban areas in Bello in Colombia, other parts of Antioquia, and the greater Rio de Janeiro area in partnership with local governments.

Scientists say once released, the infected mosquitoes breed with uninfected ones, passing on the bug to future generations.

They will monitor the programme closely for the next three years, checking to see if cases of dengue fever, Zika and chikungunya fall.

Prof Scott O'Neill, of the Eliminate Dengue Program, told the BBC: "In the communities we have already worked with there have initially been two concerns.

"One was that the mosquitoes might harm them in some way or that there might be some unintended consequences.

"It is testament to our community engagement teams working really closely with communities to answer questions that all the communities we work with are fully supportive.

"We explained Wolbachia bugs are present in so many insects worldwide that millions of humans come into contact with them everyday with no problems.

"And in the six years we have been doing these trials there have been no problems."

'Resource competition'

Researchers say it is likely that the Wolbachia approach works in two ways.

According to Prof O'Neill, Wolbachia appears to boost the immune system of mosquitoes, making them resistant to viruses like dengue.

And Wolbachia may compete with dengue and Zika for resources essential to replication. The viruses lose out and do not replicate as successfully, making it harder for them to be passed on when a mosquito bites a human.

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Scientists are planning to release an army of millions of modified mosquitoes in areas of Brazil and Colombia. They say the unusual approach is an attempt to provide "revolutionary protection" against mosquito-borne diseases such as Zika and chikungunya. The mosquitoes are infected with a bug called Wolbachia which reduces their ability to spread viruses to people.

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The fungus Piriformospora indica colonizes the roots of different plants. This can be orchids, tobacco, barley or even moss. It penetrates into the roots, but does not damage the plants. On the contrary, it can even promote the growth of its plant partners. Such and other interactions between the fungus and its partners are already known to the scientific community.

Research groups from Cologne and Würzburg are now reporting a new facet of the fungus-plant relationship in " Nature Communications": The researchers identified a protein with which the fungus suppresses the immune defence of the populated plants. So it makes sure that it is not attacked like disease-inducing fungi and the relationship can succeed in the long run.

The protein "Fungal Glucan Binding 1" (FGB1) causes, inter alia, the plant not to produce an "oxidative burst". This usually generates aggressive oxygen radicals, which destroy potential pathogens and activate the immune system of the plant.
Protein makes the plant blind to fungus structures
How does the protein lame the immune response of the plant? "It binds highly affine and very specific to sugar molecules that sit in the cell wall of the fungi and which are normally recognized as 'foreign' by the plant," explains Professor of Molecular Biology Alga Zuccaro from the University of Cologne. FGB1 acts like a camouflage coat and conceals the foreign sugar molecules from the immune system.

The relevant sugar molecules are beta-1,3 / 1,6-glucans, according to Jürgen Seibel, a professor of Organic Chemistry at the Julius-Maximilians-Universität (JMU) Würzburg. The fact that fungal glucans have a positive effect on human immune systems has been known for a long time. It is less known that they can also stimulate the immune system of plants.

The fact that the immune defence is suppressed by FGB1 in the case of Piriformospora indica, Zuccaro and Seibel can now demonstrate by combining the know-how of their working groups. The Cologne molecular biologist is an expert on root-colonizing fungi and the plant immune system, the Würzburg chemist is a specialist for sugar molecules and their functions in cells and organisms.
Perspective for medical diagnostics
The new findings may be useful in medicine and plant breeding. Given that the newly discovered protein FGB1 has such a high affinity and specificity to beta-1,6-glucans from fungi cell walls, it is possibly suitable for the diagnosis of human infections. In addition, the new knowledge could contribute to the cultivation of plants with increased disease resistance in the long term.

The next step is to examine how the plants recognize the beta-1,3 / 1,6-glucans and how exactly FGB1 suppresses them.

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How a Fungus Inhibits the Immune System of Plants - Science and Technology Research News

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The fungus Piriformospora indica colonizes the roots of different plants. This can be orchids, tobacco, barley or even moss. It penetrates into the roots, but does not damage the plants. On the contrary, it can even promote the growth of its plant partners. Such and other interactions between the fungus and its partners are already ...

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An incendiary new report from two major conservation groups predicts dire circumstances for the world's wild animals, warning that two-thirds of vertebrate populations could be wiped out by 2020, based on 1970 population levels.

The new report, called the Living Planet Index, was prepared by the World Wildlife Fund and the Zoological Society of London. The index found that animal populations dropped by 58 percent between 1970 and 2012, largely as a result of human activities, from poaching to habitat loss and pollution.

The team then extrapolated those trends forward to 2020. They based their analysis on data collected in the field on more than 14,000 populations of vertebrates, from 3,700 different species. The data came from many sources, from all around the world.

The researchers concluded that lakes and rivers saw the steepest declines in resident animals. Groups that have fared particularly badly include marine mammals, fish, and some birds ( especially vultures).

We must "act now to reform our food and energy systems and meet global commitments on addressing climate change, protecting biodiversity and supporting sustainable development," the report begins.

"Global biodiversity is declining at an alarming rate, putting the survival of other species and our own future at risk," the index warns.

But hang on, says National Geographic explorer and conservation scientist Stuart Pimm of Duke University, who was not involved with the report.

"Trying to take all those different data sets, from all over the world, and putting that in a blender and trying to break that down into one number is irresponsible," Pimm says. "That's disingenuous and not helpful."

Pimm says there is far too much variability across different regions, from the land to the sea, and too much uncertainty to predict a dire crash of all species. Further, the report "depresses people to no end, and suggests there is no hope," he says.

"But there is a lot of hope around the world," Pimm adds.

He points to the recent successes in stemming the decline of lions, tigers, and other big cats across Africa and Asia, some of which has been spearheaded by National Geographic's Big Cats Initiative, which Pimm works on.

As another example, a recent study found that coral reefs are actually doing better, and are more resilient in the face of warming seas and acidification, than scientists had thought.

Although conservationists face many challenges in protecting endangered species and their habitat, the actual issues they face are more varied and subtle than a single number of index can convey, says Pimm.

Such reports may be more about trying to grab attention and raise money than sound science, he says.

Conservation biologist Luke Dollar, who leads National Geographic's Big Cats Initiative, says he agrees with Pimm's assessment of the Living Planet Index. "That said, there's no question that a great number of populations of myriad species are in substantial decline, and will continue to demand ever-increasing efforts to stem their loss and protect the systems of which they are a part," says Dollar.

"The need for self-awareness and proactive measures to mitigate our ever-increasing impact on wildlife has also never been greater," says Dollar.
This story was updated at 6:30 pm ET with comments from Luke Dollar.

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World to Lose Two-Thirds of Wild Animals by 2020?

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An incendiary new report from two major conservation groups predicts dire circumstances for the world's wild animals, warning that two-thirds of vertebrate populations could be wiped out by 2020, based on 1970 population levels. The new report, called the Living Planet Index, was prepared by the World Wildlife Fund and the Zoological Society of London.

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For the first time, National Institutes of Health researchers have demonstrated in mice that gene therapy may be the best method for correcting the single faulty gene that causes Niemann-Pick disease, type C1 (NPC1). The gene therapy involved inserting a functional copy of the NPC1 gene into mice with the disease; the treated animals were then found to have less severe NPC1 symptoms. The study, led by researchers at NIH's National Human Genome Research Institute (NHGRI) and the Eunice Kennedy Shriver National Institute of Child Health and Human Development, was published Oct. 26, 2016, in the journal Human Molecular Genetics.

Niemann-Pick disease is a rare and fatal disorder of the central nervous system (the brain and spinal cord) that has no cure. The disease occurs when a faulty housekeeping gene fails to remove cell waste, like lipids and cholesterol. The accumulation of waste in the spleen, liver and brain causes progressive deterioration in intellectual and motor functions. It also shortens patient's lives, as people with Niemann-Pick disease typically die in their teens. There are several types of Niemann-Pick disease; this study focused on mice that had been bred with a faulty NPC1 gene to model Niemann-Pick disease, type C1.

The researchers' goal was to correct the faulty NPC1 gene in as many cells and organs as possible, with a strong focus on the brain. To do this, they used a non-disease-causing virus called the adeno-associated virus serotype 9 (AAV9)(link is external) to transfer functioning NPC1 to the cells. The AAV9 containing a functioning NPC1 gene successfully crossed the blood-brain barrier, reaching cells in the brain and elsewhere. Once inside cells, the normal NPC1 gene was then able to make the functional NPC1 protein to correct the cell defects.

With a single injection, mice showed improvements in motor coordination, weight gain and longevity compared to those without this gene therapy. The effect of gene therapy equaled that of a drug called VTS-270, which has been evaluated in preclinical and clinical studies at numerous academic labs. However, to be effective, the VTS-270 compound has to be given three times a week for the life of the mouse and does not provide a true cure. The team is now investigating if a combination of the two therapies will improve results.

"We're very encouraged by this preliminary work," said William J. Pavan, Ph.D., senior investigator in the NHGRI Genetic Disease Research Branch. "The gene therapy is treating the root of the problem, the defective gene."

"Our work in NPC1 mice may help lead to human clinical trials and eventually FDA approval for gene therapy as a treatment for NPC1 disease," said Charles P. Venditti, M.D., Ph.D., senior investigator in the NHGRI Medical Genomics and Metabolic Genetics Branch. "For NPC1 patients, gene therapy could halt progression of the disease, improve the quality of their lives and, hopefully, increase the patient's life span."

The researchers work on gene therapy for NPC1 also has the potential to treat genetic disorders with some similar features. These might include mucolipidosis IV, Batten disease and Danon disease, researchers wrote.

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Gene Therapy Shows Promise for Treating Niemann-Pick Disease Type C1 - Science and Technology Research News

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For the first time, National Institutes of Health researchers have demonstrated in mice that gene therapy may be the best method for correcting the single faulty gene that causes Niemann-Pick disease, type C1 (NPC1). The gene therapy involved inserting a functional copy of the NPC1 gene into mice with the disease; the treated animals were ...

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The Assassin Bug That Stalks Spiders on Their Own Webs

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It walks stealthily, slices through defenses, and cloaks itself in wind.

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In Brief

A new brain mapping method uses individual unique RNA strands to create "barcodes" to identify neurons.

The new method may provide new inroads to studying and treating brain conditions, such as autism, which impacts 1 in 160 children worldwide.

Mapping Complex Territory

A breakthrough method in brain mapping may help us further understand the way our brain works, and may lead to treatment for neurological issues, as well.

The neurons-the billions of cells in the brain-link to each other using electrochemical impulses, in projections called axons. Mapping the complex network of the neuron's projections let scientists gain insight on the function of specific parts of the brain, as well as researching treatments to illnesses concerning the brain.

Previously, brain mapping was usually done by infecting the neurons with viruses that glow with different colors, but this is an arduous method. Visually tracing a specific color trace takes months, and the available fluorescent proteins are limited, meaning scientists can only investigate the projections of about ten cells in a single experiment.

A new tool called Multiplexed Analysis of Projections by Sequencing (MAPseq), discussed in a study, published in the journal Neuron, from researchers in Cold Spring Harbor Laboratory, uses genetic "barcodes" instead of colors to investigate the path of the neurons. Each barcode is an RNA sequence: a unique string of protein, similar to the kind that dictates the identity of each of our own cells. Viruses transport the RNA through the neurons. In addition, the viruses still light up, allowing the researchers to see which cells have picked up a barcode.

A Projection Toward Progress

The method was tested with mice. Just two days after the RNA-carrying viruses were injected into the brainstem, the mouse brains distinctly showed networks of the neurons upon dissection and inspection under microscope.

Initial findings are already promising. The networks between the brain's area active in stress response with the brain's outer layer show underlying clues about autism. According to Spectrum, "Future versions of the tool may allow scientists to determine whether particular neuronal junctions boost or dampen brain activity." This could lead to better ways of understanding the disorder, making it easier to tailor treatments to battle it.

The brain is indeed complex territory, and studies like this bring us closer to understanding ourselves better, and more importantly, brings developments for treatment closer to reality.

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Unprecedented Brain Map Could Reveal Keys to Autism

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In Brief A new brain mapping method uses individual unique RNA strands to create "barcodes" to identify neurons. The new method may provide new inroads to studying and treating brain conditions, such as autism, which impacts 1 in 160 children worldwide.

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Labs around the world will create the most comprehensive map of the 35 trillion cells that make up the human body under plans put forward by researchers on Friday.

The international effort aims to decipher the types and properties of every cell a person contains, whether healthy or diseased, in a bid to speed up discoveries in medical science.

Named the Human Cell Atlas, the project amounts to the most concerted attempt yet to work out what we are made from and how illnesses develop when the building blocks of the body fail.

"Having an understanding of who we are is part of the human endeavour," said Aviv Regev, a computational biologist at the Broad Institute of MIT in Massachusetts. "We want to know what we are made of. But this will have a substantial impact on our scientific understanding and as a result, on our ability to diagnose, monitor and treat disease."

Many medical textbooks state that the human body contains about 200 distinct cell types, the simple biological units that build hearts and brains, livers and kidneys. But the real number is undoubtedly much higher. The light sensitive retina in a human eyeball alone holds 100 different kinds of cells. The immune system has at least twice as many as that.

"It has become clear with new technology that there are lots and lots of cell types and cell states that we know nothing about," said Sarah Teichmann, head of cellular genetics at the Sanger Institute, near Cambridge. "The Human Cell Atlas is about discovering what we're missing."

The first pilot studies to feed into the atlas have already begun. The work draws on recent technological advances that can perform detailed genetic analyses on thousands of cells a day. While most cells in the body carry the same genetic code, their fate is ruled by is the pattern of genes that is activated inside them. Switch on one group of genes and a cell becomes a neuron; activate another and it forms a beating heart cell.

Regev and Teichmann laid out plans for the atlas at a scientific meeting in London on Friday. The project has already gained support from Cori Bargmann, the incoming president of the Chan-Zuckerberg Initiative, the multibillion dollar medical research effort led by Priscilla Chan and her husband, Mark Zuckerberg.

To build up the atlas, labs around the world will work through the human body, organ by organ, and cell by cell. When these are mapped out, researchers should know not only the full variety of cells in the body, but also where they are found in a person's organs.

Regev believes the project will impact on almost every aspect of medicine and biology for decades to come. Armed with a full list of immune cells in the body, scientists might devise new therapies to tackle autoimmune diseases, such as multiple sclerosis, and block the body's rejection of implanted organs.

Sten Linnarsson, a neuroscientist at the Karolinska Institute in Stockholm, said the atlas could prove invaluable for cell-based therapies that aim to regenerate lost or damaged tissues. For example, Parkinson's disease is caused by the steady loss of neurons that produce a chemical called dopamine in the brain. One hope for a future therapy is to grow fresh dopamine-making cells in the lab, and then inject them into the brain. A cell atlas would help reassure scientists they had grown the right cells to implant. "If you're going to put them into people's brains, you have to be pretty sure what they are," he said.

"The Human Cell Atlas is the most exciting initiative to come out of the life science community in a long time," Linnarsson said. "In sickness and in health, cells are the fundamental units of life, and only by knowing our cells will we be able to fully comprehend the mechanisms of human disease."
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Human Cell Atlas project aims to map the human body's 35 trillion cells

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Labs around the world will create the most comprehensive map of the 35 trillion cells that make up the human body under plans put forward by researchers on Friday. The international effort aims to decipher the types and properties of every cell a person contains, whether healthy or diseased, in a bid to speed up discoveries in medical science.

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Pardis Sabeti is a computational geneticist who works at the Broad Institute of MIT Harvard, where she pinpoints the genetic factors in genomes that allow diseases to take hold.

When the Ebola outbreak struck in 2014, Sabeti worked between a clinic in Kenema, Sierra Leone, and her lab in Harvard to sequence the virus's genomes. Her lab mined the samples for clues about how it evolves and spreads. As they worked, they put the data online, free to use, to help drive the development of diagnostics and treatments. At the time, the first batch of 99 genomes sequenced made up the biggest published dataset on Ebola.

Sabeti has become an advocate for sharing data online to speed up response. Here she tells WIRED about how Ebola survivors have become a focus of her research, and a new open-access app that will improve diagnosis of infected patients.

WIRED: What are your lab's central aims?

Pardis Sabeti: One of our strengths is computational biology: taking genomes and trying to understand what's meaningful and what changes have been important. I look at the human and viral sides, and both have a lot to offer - for instance, tracing the human genome to understand what were the major pressures on it, and in doing so, pointing to things we didn't know about that are important. We're mining the genome for clues.

Why gather data on viruses such as Ebola or Lassa?

Everything we do is based on the genome sequences of a virus. All sorts of data need to be available - clinical data, genomic data, epidemiological data. But when it comes to genome data, you need it for everything: the diagnostics; the vaccines; and the therapies. These are our major action items in the lab.

A major focus for you has been making genetic data on Ebola freely available. Has this led to any breakthroughs?

Of the things I've done in my career that have made me most proud, it was when we released this data. Many people have since told me how they have developed a new diagnostic based on our sequences1. Knowing that was made possible was a big deal. Some vaccines were developed using it too. Vaccines and diagnostics are practical things which we know more data will allow to be as good as they can be.

What's the status of your genome-sequencing work?

It's continuing. As new cases emerge we're sequencing them to understand where they might have come from and how they might relate to others. Also, there is an interesting case of individuals who are likely reservoirs for the virus. They have Ebola in their semen and in their breast milk, and that's frightening. People will say: "Oh, they survived Ebola," but with both Lassa and Ebola the long-term effects on health are dramatic. It's something we need to work on to stop. We're trying to understand what the viral population is in these people and how it is changing.

You've also built an app called Ebola CARE that predicts patients' outcomes based on symptoms. How does it work?

Using a small clinical data set from Ebola patients during the West African outbreak, we developed a statistical method that's expected to help clinicians predict a new patient's prognosis - their probability of fatality or recovery - to nearly 100 per cent accuracy2. To make it available in the field we've made the mobile app and the algorithms behind it open and flexible to being updated with better data, to encourage others to make outbreak data open access. If we can create tools that give clinicians real-time information, they're likely to put data into a system that other people can access. They can help drive research.

You've also been working on the Zika virus. Is this building on your Ebola research?

The technologies we've been developing for Ebola work well for many viruses, but Zika is more challenging as it often occurs at very low concentrations in patient samples.

Zika: how can it be stopped?

For this reason, researchers have only been able to sequence a small number of samples over the past year, leaving many questions about the virus's evolution and diversity.

My lab has been developing technologies to sequence the Zika virus.

The technology is ready; our challenge is finding collaborators. We welcome anyone who'd like to work with us.

Do you think the push for transparency and data sharing during the Ebola epidemic has changed the conversation around outbreak response?

There's definitely been a sea change, with a great deal of messaging now about open access and sharing data. But we need to work to make sure that we follow this not just in our language but in our actions and beliefs. These situations in an outbreak can be fast-moving and we are in a race against time. We need to figure out how to move things forward, because this was a major warning to the world - but it's not the worst we have or could see.

1. Stephen K. Gire, 2014. "Genomic surveillance elucidates Ebola virus origin and transmission during the 2014 outbreak," Science 6202, 1369-1372

2. Andres Colubri, 2016. "Transforming Clinical Data into Actionable Prognosis Models: Machine-Learning Framework and Field-Deployable App
to Predict Outcome of Ebola Patients," Public Library of Science Neglected Tropical Diseases

This article was first published in the October 2016 issue of WIRED magazine

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A cure for Zika may lie in mining viruses for genetic data

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Pardis Sabeti is a computational geneticist who works at the Broad Institute of MIT Harvard, where she pinpoints the genetic factors in genomes that allow diseases to take hold. When the Ebola outbreak struck in 2014, Sabeti worked between a clinic in Kenema, Sierra Leone, and her lab in Harvard to sequence the virus's genomes.

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They are creepy, crawly and, for some, a source of irrational fear. Now scientists have found that spiders can hear you from across a room.

The discovery came as a surprise because, technically, spiders do not have ears. However, the latest research shows that the hairs on spiders' legs are so sensitive that they can detect human speech from several metres away.

Paul Shamble, an arachnologist who led the research at Cornell University, said that the finding is exciting because it overturns the idea that the world of arachnids is dominated by sight and touch.

"Surprisingly, we found that they also possess an acute sense of hearing," he said. "They can hear sounds at distances much farther away than previously thought, even though they lack ears with the eardrums typical of most animals with long-distance hearing."

"I'm not sure that everyone's going to be thrilled that spiders can hear them as well see them," he added.

Shamble and colleagues made the discovery after succeeding in making direct electrical recordings from the brains of North American jumping spiders. This was a technical feat because the spider's body is pressurised like an inflated tyre, meaning that previous attempts to record from their brains typically caused the spider to explode as soon as a hole was drilled in the outer shell.

The team had initially been investigating how the creatures process visual information, but noticed that their brains were responding when chair were moved around the lab or one of the team clapped their hands.

"That was remarkable because the received wisdom at that point was that spiders can't hear sounds," said Prof Ronald Hoy, senior author of the paper, which is published in Current Biology.

The spiders' sense of hearing appeared to rely on tiny hairs on their forelegs - when the scientists placed water droplets on the spiders' legs to dull the vibrations of the hairs, the auditory neurons in the brain stopped firing in response to sounds.

Further investigation showed the spiders could hear claps from more than five metres away and that they were most sensitive to low frequencies (about 80-130Hz), which would match the wingbeats of parasitoid wasps, a predator of jumping spiders, or the pitch of a very deep male voice.

The overall sensory experience would probably be a lot less rich than that of humans. "It probably sounds like a really bad phone connection," said Shamble. "They probably can tell that you're talking from across the room, but they're certainly not listening to you."

The researchers believe that other spider species are likely to have similar hearing abilities are now recording from the brains of fishing spiders, wolf spiders, and others.
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Spiders don't have ears - but they can still hear you coming

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They are creepy, crawly and, for some, a source of irrational fear. Now scientists have found that spiders can hear you from across a room. The discovery came as a surprise because, technically, spiders do not have ears. However, the latest research shows that the hairs on spiders' legs are so sensitive that they can detect human speech from several metres away.

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Bees are capable of learning and teaching new skills, just like humans

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Don't underestimate the tiny brain of a bee. Turns out, bees have more complex cognitive and learning skills than we previously thought. Scientists from the Queen Mary University of London taught bees to pull string for food. These bees then went on to teach others to do the same thing.

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Ellen Jorgensen: What you need to know about CRISPR

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Should we bring back the wooly mammoth? Or edit a human embryo? Or wipe out an entire species that we consider harmful? The genome-editing technology CRISPR has made extraordinary questions like these legitimate -- but how does it work?

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BIRD migration is an extraordinary thing, in fact, in some cases, it verges on the unbelievable. Every autumn Aleutian bar-tailed godwits fly non-stop for nine days from Alaska to New Zealand, a distance of more than 11,000km.

Great shearwaters and sooty shearwaters, which are flying off our coasts at present, were hatched on remote islands in the Roaring Forties of the southern hemisphere. Miniature tracking devices attached to some have revealed that in the course of their world travels they fatten up on Canada's Grand Banks and don't feed again until they arrive off the east coast of Argentina.

Many long-distance migrants prepare for the journey by undergoing changes that seem as miraculous as Clark Kent's transformation into Superman. All their non-vital organs, including their digestive systems, shrink in order to reduce weight and make space for the fat that fuels the flight. They reconfigure the amount of haemoglobin in their bloodstream so they can fly at high altitudes where the air is thin but there are beneficial tail winds. All this so that they can enjoy perpetual summer by flying from one hemisphere to another.

Not all bird migration is as dramatic as this and some of it is far from obvious. For the next few months you won't notice anything different about the blackbirds in your garden but most of them will actually hail from Scandinavia, the Baltic countries and even further east. The same is true of winter starling flocks.

Autumn is a busy season for Irish twitchers trying to add a new species to their life list. Ireland, off the Atlantic seaboard of Europe, is geographically well placed to receive what ornithologists call vagrants - birds that have strayed from their normal migration route.

We tend to think of a vagrant as a bird that's made a mistake. It might be more accurate to think of them as pioneers or explorers testing out new possibilities and future migration routes. Patterns of migration are continually evolving. Fifty years ago the blackcaps of central Europe all went south in winter. Then some pioneering individuals went west and ended up in Ireland. Nowadays wintering blackcaps are common Irish garden birds.

The question of how migrating birds navigate, often across featureless oceans or deserts, is one that has attracted many theories and practically no hard facts. There probably isn't one single answer to fit the many different patterns of migration. Some travel at night, leading to theories that they use the position of the stars to establish direction. Others travel by day, and still more by both day and night, and it's been suggested that they use the earth's magnetic field.

Scientists are rather bad at admitting defeat, but how migrating birds navigate is a mystery.

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Scientists still mystified by bird migration

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BIRD migration is an extraordinary thing, in fact, in some cases, it verges on the unbelievable. Every autumn Aleutian bar-tailed godwits fly non-stop for nine days from Alaska to New Zealand, a distance of more than 11,000km. Great shearwaters and sooty shearwaters, which are flying off our coasts at present, were hatched on remote islands in the Roaring Forties of the southern hemisphere.

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The RNA world hypothesis

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You can now support us on Patreon! https://www.patreon.com/statedclearly All living creatures today reproduce and evolve using a complex gene-enzyme cycle. If we look at a cell, for example, information encoded in its genes is used to produce functional proteins called enzymes.

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The Primitive Streak | Radiolab | WNYC Studios

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In a recent breakthrough, researchers grew human embryos longer than ever before, witnessing a mysterious part of human development, and crashing into a decades-old ethical dilemma.

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In Brief

Scientists have been studying several ant species that could be the key to combating antibiotic resistance. These ants have a symbiotic relationship with organisms that create compounds that protect the ants against fungi, bacteria, and microbes.

A Symbiotic Relationship

Antibiotic resistance is a huge crisis currently threatening the whole world. In fact, it's such a big deal that it's even being discussed by the UN General Assembly. According to estimates, more than 700,000 people die of drug-resistant infections each year across the globe, and bad bacteria continue to evolve against the treatments that do work.

To help alleviate that problem, researchers are looking for answers in the unlikeliest of places: the backs of ants.

Scientists have found ants that cultivate bacteria they can use against invading fungi and microbes, and it could be a potential new source for antibiotics. Researchers have narrowed down the search for these special ants to species that cultivate fungi as their food source, such as leaf-cutter ants, which are found in North and South America.

The leaf-cutter ants bring leaves back to their nests and leave them on the ground for fungi to decompose. The fungi then becomes a food source for the ants. All is well until other fungi types start invading the nest's turf, killing both the ants and the farmed fungi. To protect themselves, the ants enter a symbiotic relationship with certain bacteria that excrete antibiotic and antifungal compounds. These bacteria look like powdered sugar sprinkled on the ants' backs.

This war between the ants and the detrimental fungi has been going on for millions of years, so the techniques and compounds the ants use have had time to be refined and improved upon. This gives researchers a solid basis on which to test out new ideas on the most-effective compounds to use to make our own medicines to fight antibiotic resistance.

New Avenues For Treatments

Research of this kind has actually been going on since the '90s, and not only has it yielded antibiotic and antifungal treatments, but the original studies also explored whether researchers could use the ants to develop anti-cancer and antiparasitic drugs.

This line of research highlights the variety of unlikely places scientists have been looking for answers to solve this superbug crisis. Apart from developing new drugs, researchers have also been exploring the use of viruses to kill bacteria and even nanotechnology solutions to combat drug-resistant bacteria.

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One Superbug Meets Another: Ants Could Be the Key to Battling Antibiotic Resistance

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In Brief Scientists have been studying several ant species that could be the key to combating antibiotic resistance. These ants have a symbiotic relationship with organisms that create compounds that protect the ants against fungi, bacteria, and microbes. Antibiotic resistance is a huge crisis currently threatening the whole world.

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Out of the belly of a bright orange frog, a mysterious species of ant appears.

Scientists discovered the Lenomyrmex hoelldobleri ant in the stomach of a dendrobatid frog, Oophaga sylvatica--known as diablito--in northwestern Ecuador.

To gather clues about their diet and environment, researchers capture tropical frogs and flush their stomachs to make them vomit their lunch, then release them unscathed back into the wild. University of Rochester myrmecologist Christian Rabeling and colleagues used this method on tropical frogs. The frog is neon-orange and poisonous. It's believed that their toxic secretions are thanks to a steady diet of ants, whose own diets contain alkaloids from plants. These alkaloids play a part in how poison dart frogs convert their own snacks into deadly defense mechanisms against larger predators.

The ant's taxonomy, as outlined in their report published in ZooKeys, is filled with such koans as "Compound eyes large, protruding." "Tarsal claws simple, elongated." "Mandibles smooth, slightly shining." It's named for Bert Hölldobler's 80th birthday, who has a "passion for ants."

How, exactly, L. hoelldobleri affects the frog's poisonous nature and how the ants carry on life in the wild is still a mystery, since the only ones scientists have seen so far are these poor barfed-up specimens.

[H/T National Geographic]

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A Devil Frog Puked Up This New Ant Species

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Out of the belly of a bright orange frog, a mysterious species of ant appears. Scientists discovered the Lenomyrmex hoelldobleri ant in the stomach of a dendrobatid frog, Oophaga sylvatica--known as diablito--in northwestern Ecuador. To gather clues about their diet and environment, researchers capture tropical frogs and flush their stomachs to make them vomit their lunch, then release them unscathed back into the wild.

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Automating forestry is an uphill battle. Trees grow well on slopes and steep inclines, which are difficult for farming equipment, adapted as it is to sweeping, gentle plains. This is especially hard for the replanting part of responsible forestry, where seedlings need deliberate, tender care so they can begin to replace their fallen predecessors. This is, right now, a human intensive process, but startup DroneSeed wants to turn over the entire process to, you guessed it, drones.

Besides the private forestry industry, another, more immediate need might take advantage of the DroneSeed technology: reseeding after forest fires. Motherboard reports:

Forestry industry chatter suggests aerial seeding isn't ready, not amidst the stumps and slash leftover from a timber harvest. But burn zones might be another story. Ullyott thinks that his company can speed up the remediation of charred forests. "I'm personally really excited about that," he said. Quick replanting is crucial for habitats and budgets, but the slower process of using seedlings has a proven success rate. DroneSeed will need to prove itself by proving the viability of their seeds.

DroneSeed has drones that can launch seeds, spray herbicide on invasive species, and monitor plant growth. The easy part is flying over the cut. The tricky part is making sure that the drone-planted seeds take.

Still, given the challenges in replanting by hand, drones are at worst a novel attempt at a solution. And if the seeds sprout and thrive, and the FAA approves DroneSeed's operation, then a new way of forestry could take root.

Watch below:

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DroneSeed Company Could Replant Burned Forests

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Automating forestry is an uphill battle. Trees grow well on slopes and steep inclines, which are difficult for farming equipment, adapted as it is to sweeping, gentle plains. This is especially hard for the replanting part of responsible forestry, where seedlings need deliberate, tender care so they can begin to replace their fallen predecessors.

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Podcast about the mutualism between plants and fungi.

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From Tree to Shining Tree

(Photo Credit: Flickred!/Flickr)

A forest can feel like a place of great stillness and quiet. But if you dig a little deeper, there's a hidden world beneath your feet as busy and complicated as a city at rush hour.

In this story, a dog introduces us to a strange creature that burrows beneath forests, building an underground network where deals are made and lives are saved (and lost) in a complex web of friendships, rivalries, and business relations. It's a network that scientists are only just beginning to untangle and map, and it's not only turning our understanding of forests upside down, it's leading some researchers to rethink what it means to be intelligent.
Produced by Annie McEwen and Brenna Farrell. Special Thanks to Latif Nasser, Stephanie Tam, Teresa Ryan, Marc Guttman, and Professor Nicholas P. Money at Miami University. Correction: An earlier version of this story misidentified naturalist David Attenborough as his late brother, actor Richard Attenborough. In addition, it dated the earliest scientific studies of fungi to the late 19th century, whereas naturalists have studied fungi since the 17th century. Lastly, we mistakenly stated that the oxygen that a plant respires comes from CO2, when in reality it comes from water. The audio has been adjusted to correct these facts.
Support Radiolab by becoming a member today at Radiolab.org/donate.

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From Tree to Shining Tree (Photo Credit: Flickred!/Flickr) A forest can feel like a place of great stillness and quiet. But if you dig a little deeper, there's a hidden world beneath your feet as busy and complicated as a city at rush hour.

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Stem Cells Magnet Could Help Heal Bones - Financial Tribune

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Tiny bundles of stem cells built in the laboratory using microscopic magnets could pave...

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Giant 'corpse flower' begins to bloom for first time in five years - the guardian

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Endangered plant named 'morphy' starts to smell like a burning cigar at Ivy League college but far worse whiffs lie in store at the weekend

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Speaking with: Bad Pharma author Ben Goldacre about how bad research hurts us all | Australasian Science Magazine - Australasian Science

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Shutterstock We are living in a time where we have greater access to lifesaving medicines and treatments than ever before.

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Interesting article

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Reef Fish Sing In The Morning, Just Like Birds | Care2 Causes - Care2

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We've long admired the ever popular songs of humpback whales, and questioned what the various clicks and whistles other marine animals use to communicate mean,

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Great podcast about the world wide web

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From Tree to Shining Tree

(Photo Credit: Flickred!/Flickr)

A forest can feel like a place of great stillness and quiet. But if you dig a little deeper, there's a hidden world beneath your feet as busy and complicated as a city at rush hour.

In this story, a dog introduces us to a strange creature that burrows beneath forests, building an underground network where deals are made and lives are saved (and lost) in a complex web of friendships, rivalries, and business relations. It's a network that scientists are only just beginning to untangle and map, and it's not only turning our understanding of forests upside down, it's leading some researchers to rethink what it means to be intelligent.
Produced by Annie McEwen and Brenna Farrell. Special Thanks to Latif Nasser, Stephanie Tam, Teresa Ryan, Marc Guttman, and Professor Nicholas P. Money at Miami University. Correction: An earlier version of this story misidentified naturalist David Attenborough as his late brother, actor Richard Attenborough. In addition, it dated the earliest scientific studies of fungi to the late 19th century, whereas naturalists have studied fungi since the 17th century. Lastly, we mistakenly stated that the oxygen that a plant respires comes from CO2, when in reality it comes from water. The audio has been adjusted to correct these facts.
Support Radiolab by becoming a member today at Radiolab.org/donate.

# data[].attributes.attachment_link.description
From Tree to Shining Tree (Photo Credit: Flickred!/Flickr) A forest can feel like a place of great stillness and quiet. But if you dig a little deeper, there's a hidden world beneath your feet as busy and complicated as a city at rush hour.

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14/09/2016, The Waterside Ape - BBC Radio 4

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Sir David Attenborough examines new evidence on a controversial theory of human origins.