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This website describes what the cell cycle is, along with each of the steps in depth. It also gives some photos for examples of the steps, and provides additional facts about the process.

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Phases of the cell cycle (article) | Khan Academy

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Learn for free about math, art, computer programming, economics, physics, chemistry, biology, medicine, finance, history, and more. Khan Academy is a nonprofit with the mission of providing a free, world-class education for anyone, anywhere.

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This Amoeba Sisters video describes the cell cycle, and provides some information about cancer, too.

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This is a diagram of the cell cycle, including a short description of each phase.

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This website describes the checkpoints that control the cell cycle internally, as well as what positive and negative regulator molecules do. It also includes an animation to show the checkpoints.

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Learning Objectives

By the end of this section, you will be able to:

Understand how the cell cycle is controlled by mechanisms both internal and external to the cell

Explain how the three internal control checkpoints occur at the end of G₁, at the G₂/M transition, and during metaphase

Describe the molecules that control the cell cycle through positive and negative regulation

The length of the cell cycle is highly variable, even within the cells of a single organism. In humans, the frequency of cell turnover ranges from a few hours in early embryonic development, to an average of two to five days for epithelial cells, and to an entire human lifetime spent in G ₀ by specialized cells, such as cortical neurons or cardiac muscle cells. There is also variation in the time that a cell spends in each phase of the cell cycle. When fast-dividing mammalian cells are grown in culture (outside the body under optimal growing conditions), the length of the cycle is about 24 hours. In rapidly dividing human cells with a 24-hour cell cycle, the G ₁ phase lasts approximately nine hours, the S phase lasts 10 hours, the G ₂ phase lasts about four and one-half hours, and the M phase lasts approximately one-half hour. In early embryos of fruit flies, the cell cycle is completed in about eight minutes. The timing of events in the cell cycle is controlled by mechanisms that are both internal and external to the cell.

Regulation of the Cell Cycle by External Events

Both the initiation and inhibition of cell division are triggered by events external to the cell when it is about to begin the replication process. An event may be as simple as the death of a nearby cell or as sweeping as the release of growth-promoting hormones, such as human growth hormone (HGH). A lack of HGH can inhibit cell division, resulting in dwarfism, whereas too much HGH can result in gigantism. Crowding of cells can also inhibit cell division. Another factor that can initiate cell division is the size of the cell; as a cell grows, it becomes inefficient due to its decreasing surface-to-volume ratio. The solution to this problem is to divide.

Whatever the source of the message, the cell receives the signal, and a series of events within the cell allows it to proceed into interphase. Moving forward from this initiation point, every parameter required during each cell cycle phase must be met or the cycle cannot progress.

Regulation at Internal Checkpoints

It is essential that the daughter cells produced be exact duplicates of the parent cell. Mistakes in the duplication or distribution of the chromosomes lead to mutations that may be passed forward to every new cell produced from an abnormal cell. To prevent a compromised cell from continuing to divide, there are internal control mechanisms that operate at three main cell cycle checkpoints. A checkpoint is one of several points in the eukaryotic cell cycle at which the progression of a cell to the next stage in the cycle can be halted until conditions are favorable. These checkpoints occur near the end of G ₁, at the G ₂/M transition, and during metaphase (Figure 1).

The G₁ Checkpoint

The G ₁ checkpoint determines whether all conditions are favorable for cell division to proceed. The G ₁ checkpoint, also called the restriction point (in yeast), is a point at which the cell irreversibly commits to the cell division process. External influences, such as growth factors, play a large role in carrying the cell past the G ₁ checkpoint. In addition to adequate reserves and cell size, there is a check for genomic DNA damage at the G ₁ checkpoint. A cell that does not meet all the requirements will not be allowed to progress into the S phase. The cell can halt the cycle and attempt to remedy the problematic condition, or the cell can advance into G ₀ and await further signals when conditions improve.

The G₂ Checkpoint

The G ₂ checkpoint bars entry into the mitotic phase if certain conditions are not met. As at the G ₁ checkpoint, cell size and protein reserves are assessed. However, the most important role of the G ₂ checkpoint is to ensure that all of the chromosomes have been replicated and that the replicated DNA is not damaged. If the checkpoint mechanisms detect problems with the DNA, the cell cycle is halted, and the cell attempts to either complete DNA replication or repair the damaged DNA.

The M Checkpoint

The M checkpoint occurs near the end of the metaphase stage of karyokinesis. The M checkpoint is also known as the spindle checkpoint, because it determines whether all the sister chromatids are correctly attached to the spindle microtubules. Because the separation of the sister chromatids during anaphase is an irreversible step, the cycle will not proceed until the kinetochores of each pair of sister chromatids are firmly anchored to at least two spindle fibers arising from opposite poles of the cell.

Regulator Molecules of the Cell Cycle

In addition to the internally controlled checkpoints, there are two groups of intracellular molecules that regulate the cell cycle. These regulatory molecules either promote progress of the cell to the next phase (positive regulation) or halt the cycle (negative regulation). Regulator molecules may act individually, or they can influence the activity or production of other regulatory proteins. Therefore, the failure of a single regulator may have almost no effect on the cell cycle, especially if more than one mechanism controls the same event. Conversely, the effect of a deficient or non-functioning regulator can be wide-ranging and possibly fatal to the cell if multiple processes are affected.

Positive Regulation of the Cell Cycle

Two groups of proteins, called cyclins and cyclin-dependent kinases (Cdks), are responsible for the progress of the cell through the various checkpoints. The levels of the four cyclin proteins fluctuate throughout the cell cycle in a predictable pattern (Figure 2). Increases in the concentration of cyclin proteins are triggered by both external and internal signals. After the cell moves to the next stage of the cell cycle, the cyclins that were active in the previous stage are degraded.

Cyclins regulate the cell cycle only when they are tightly bound to Cdks. To be fully active, the Cdk/cyclin complex must also be phosphorylated in specific locations. Like all kinases, Cdks are enzymes (kinases) that phosphorylate other proteins. Phosphorylation activates the protein by changing its shape. The proteins phosphorylated by Cdks are involved in advancing the cell to the next phase. (Figure 3). The levels of Cdk proteins are relatively stable throughout the cell cycle; however, the concentrations of cyclin fluctuate and determine when Cdk/cyclin complexes form. The different cyclins and Cdks bind at specific points in the cell cycle and thus regulate different checkpoints.

Since the cyclic fluctuations of cyclin levels are based on the timing of the cell cycle and not on specific events, regulation of the cell cycle usually occurs by either the Cdk molecules alone or the Cdk/cyclin complexes. Without a specific concentration of fully activated cyclin/Cdk complexes, the cell cycle cannot proceed through the checkpoints.

Although the cyclins are the main regulatory molecules that determine the forward momentum of the cell cycle, there are several other mechanisms that fine-tune the progress of the cycle with negative, rather than positive, effects. These mechanisms essentially block the progression of the cell cycle until problematic conditions are resolved. Molecules that prevent the full activation of Cdks are called Cdk inhibitors. Many of these inhibitor molecules directly or indirectly monitor a particular cell cycle event. The block placed on Cdks by inhibitor molecules will not be removed until the specific event that the inhibitor monitors is completed.

Negative Regulation of the Cell Cycle

The second group of cell cycle regulatory molecules are negative regulators. Negative regulators halt the cell cycle. Remember that in positive regulation, active molecules cause the cycle to progress.

The best understood negative regulatory molecules are retinoblastoma protein (Rb), p53, and p21. Retinoblastoma proteins are a group of tumor-suppressor proteins common in many cells. The 53 and 21 designations refer to the functional molecular masses of the proteins (p) in kilodaltons. Much of what is known about cell cycle regulation comes from research conducted with cells that have lost regulatory control. All three of these regulatory proteins were discovered to be damaged or non-functional in cells that had begun to replicate uncontrollably (became cancerous). In each case, the main cause of the unchecked progress through the cell cycle was a faulty copy of the regulatory protein.

Rb, p53, and p21 act primarily at the G ₁ checkpoint. p53 is a multi-functional protein that has a major impact on the commitment of a cell to division because it acts when there is damaged DNA in cells that are undergoing the preparatory processes during G ₁. If damaged DNA is detected, p53 halts the cell cycle and recruits enzymes to repair the DNA. If the DNA cannot be repaired, p53 can trigger apoptosis, or cell suicide, to prevent the duplication of damaged chromosomes. As p53 levels rise, the production of p21 is triggered. p21 enforces the halt in the cycle dictated by p53 by binding to and inhibiting the activity of the Cdk/cyclin complexes. As a cell is exposed to more stress, higher levels of p53 and p21 accumulate, making it less likely that the cell will move into the S phase.

Rb exerts its regulatory influence on other positive regulator proteins. Chiefly, Rb monitors cell size. In the active, dephosphorylated state, Rb binds to proteins called transcription factors, most commonly, E2F (Figure 4). Transcription factors "turn on" specific genes, allowing the production of proteins encoded by that gene. When Rb is bound to E2F, production of proteins necessary for the G ₁/S transition is blocked. As the cell increases in size, Rb is slowly phosphorylated until it becomes inactivated. Rb releases E2F, which can now turn on the gene that produces the transition protein, and this particular block is removed. For the cell to move past each of the checkpoints, all positive regulators must be "turned on," and all negative regulators must be "turned off."

Rb and other proteins that negatively regulate the cell cycle are sometimes called tumor suppressors. Why do you think the name tumor suppressor might be appropriate for these proteins?

Section Summary

Each step of the cell cycle is monitored by internal controls called checkpoints. There are three major checkpoints in the cell cycle: one near the end of G ₁, a second at the G ₂/M transition, and the third during metaphase. Positive regulator molecules allow the cell cycle to advance to the next stage. Negative regulator molecules monitor cellular conditions and can halt the cycle until specific requirements are met.

Additional Self Check Questions

1. Rb and other proteins that negatively regulate the cell cycle are sometimes called tumor suppressors. Why do you think the name tumor suppressor might be an appropriate for these proteins?

2. Describe the general conditions that must be met at each of the three main cell cycle checkpoints.

3. Explain the roles of the positive cell cycle regulators compared to the negative regulators.

4. What steps are necessary for Cdk to become fully active?

5. Rb is a negative regulator that blocks the cell cycle at the G ₁ checkpoint until the cell achieves a requisite size. What molecular mechanism does Rb employ to halt the cell cycle?

Answers

1. Rb and other negative regulatory proteins control cell division and therefore prevent the formation of tumors. Mutations that prevent these proteins from carrying out their function can result in cancer.

2. The G ₁ checkpoint monitors adequate cell growth, the state of the genomic DNA, adequate stores of energy, and materials for S phase. At the G ₂ checkpoint, DNA is checked to ensure that all chromosomes were duplicated and that there are no mistakes in newly synthesized DNA. Additionally, cell size and energy reserves are evaluated. The M checkpoint confirms the correct attachment of the mitotic spindle fibers to the kinetochores.

3. Positive cell regulators such as cyclin and Cdk perform tasks that advance the cell cycle to the next stage. Negative regulators such as Rb, p53, and p21 block the progression of the cell cycle until certain events have occurred.

4. Cdk must bind to a cyclin, and it must be phosphorylated in the correct position to become fully active.

5. Rb is active when it is dephosphorylated. In this state, Rb binds to E2F, which is a transcription factor required for the transcription and eventual translation of molecules required for the G ₁/S transition. E2F cannot transcribe certain genes when it is bound to Rb. As the cell increases in size, Rb becomes phosphorylated, inactivated, and releases E2F. E2F can then promote the transcription of the genes it controls, and the transition proteins will be produced.

Glossary

cell cycle checkpoint: mechanism that monitors the preparedness of a eukaryotic cell to advance through the various cell cycle stages

cyclin: one of a group of proteins that act in conjunction with cyclin-dependent kinases to help regulate the cell cycle by phosphorylating key proteins; the concentrations of cyclins fluctuate throughout the cell cycle

cyclin-dependent kinase: one of a group of protein kinases that helps to regulate the cell cycle when bound to cyclin; it functions to phosphorylate other proteins that are either activated or inactivated by phosphorylation

p21: cell cycle regulatory protein that inhibits the cell cycle; its levels are controlled by p53

p53: cell cycle regulatory protein that regulates cell growth and monitors DNA damage; it halts the progression of the cell cycle in cases of DNA damage and may induce apoptosis

retinoblastoma protein (Rb): regulatory molecule that exhibits negative effects on the cell cycle by interacting with a transcription factor (E2F)

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By the end of this section, you will be able to: Understand how the cell cycle is controlled by mechanisms both internal and external to the cell Explain how the three internal control checkpoints occur at the end of G1, at the G2/M transition, and during metaphase Describe the molecules that control the cell cycle through positive and negative regulation The length of the cell cycle is highly variable, even within the cells of a single organism.

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A short video by Khan Academy reviewing how the cell cycle is controlled.

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Now, the cell cycle is not the sort of thing that occurs in a very unchecked manner. There's actually a lot of regulation in play here. In fact, there are two key places that we have extensive regulation of the cell cycle. The first check point is right here between the G1 and the S phase. So, we regulate before we get to the point of DNA replication. The other major checkpoint is right here, between G2 and the step where we jump right to mitosis. And, there are a couple of proteins that regulate this process. Two main ones are called cyclin-dependent kinases, which as you may recall, a kinase is something that adds a phosphate group. So I'll put a plus in parentheses. It will plus a phosphate group. And it will add a phosphate group on other enzymes or proteins to either activate or inactivate them. These cyclin-dependent kinases will work together with a protein you might be able to guess the name of: cyclins! Right? Because what else would these kinases depend on? So an important thing to notice is that these cyclin-dependent kinases, or CDKs, are always present. All the different types are always present in a cell, but their default form, or their default function, is for them to be inactive. And so they need to be activated by these cyclin proteins. And the point of regulation here is that specific cyclins... I'll just write, "spec," are made at specific times. And again, the reason why they're both so important is that when you have a cyclin-dependent kinase, it is only active when it is bound to a specific cyclin. It's at this point, again, that this guy is active, and the CDK is the business-end of this complex. So that's the reason why in G1 you'll see the production of cyclins D and E. >From there you will see CDK-2 bound to your cyclin E, and at the same time you'll also have your CDK-4 bound to your cyclin D. These activated kinases, then, specifically the CDK-4 cyclin D complex, will phosphorylate a protein called, "RB." So I'll draw just a little reaction over here where we add a phosphate group on our RB protein. So when RB is phosphorylated, it can't inhibit DNA replication, like it usually is supposed to do. The phosphate group renders it inactive. And this is sort of the set up we have as we go further on in our cell cycle. In the S phase we have cyclin A produced. Cyclin A will complex, again, with CDK-2 most directly to activate DNA replication, so it helps to activate DNA replication and in a similar way we have cyclin B only produced in the G2 phase, because the cyclin B CDK-1 complex is able to activate what step, do you think? Mitosis, or cell division. So, it's important to recognize that in order to pass these checkpoints, you need to have these cyclin proteins present so that they can go ahead and inhibit proteins that are blocking DNA synthesis or replication from occurring, or so they can promote the production of proteins that are needed for mitosis.

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Cell cycle control (video) | Khan Academy

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Visit us (http://www.khanacademy.org/science/healthcare-and-medicine) for health and medicine content or (http://www.khanacademy.org/test-prep/mcat) for MCAT related content. These videos do not provide medical advice and are for informational purposes only. The videos are not intended to be a substitute for professional medical advice, diagnosis or treatment.

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This website provides a video describing sexual and asexual reproduction, as well as a second part of the website describing the two types with diagrams and pictures.

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If you're seeing this message, it means we're having trouble loading external resources on our website.

If you're behind a web filter, please make sure that the domains *.kastatic.org and *.kasandbox.org are unblocked.

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Asexual and sexual reproduction (video) | Khan Academy

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This website describes cancer, its five main types, and how to treat it, along with a video to watch on the subject.

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Cancer is the uncontrolled growth of abnormal cells in the body. Cancer develops when the body's normal control mechanism stops working. Old cells do not die and instead grow out of control, forming new, abnormal cells. These extra cells may form a mass of tissue, called a tumor. Some cancers, such as leukemia, do not form tumors.

How common is cancer?

For decades, the overall rate of new cases in the United States has been trending slowly downward, but that doesn't mean that cancer is now uncommon. In fact, according to the National Cancer Institute, about 39.5 percent of all men and women in the United States will be diagnosed with cancer at some point in their lives.

Some cancers are more common than others, with the following cited as the most prevalent nationwide currently:

While the rate of most cancers is trending downward, the rate of certain types, such as melanoma, has actually increased in the past few decades.

What are the most common forms of cancer?

Cancer may occur anywhere in the body. In women, breast cancer is one of the most common. In men, it's prostate cancer. Lung cancer and colorectal cancer affect both men and women in high numbers.

There are five main categories of cancer:

Carcinomas begin in the skin or tissues that line the internal organs.

Sarcomas develop in the bone, cartilage, fat, muscle or other connective tissues.

Leukemia begins in the blood and bone marrow.

Lymphomas start in the immune system.

Central nervous system cancers develop in the brain and spinal cord.

How do you get cancer?

Experts don't yet have all the answers about what causes cancer. There are, however, certain characteristics-called risk factors -that may increase your likelihood of developing cancer.

You can control some risk factors (smoking, for example), but not others (like your race or age). Moreover, some cancers can be caused by factors in your environment, such as exposure to the ultraviolet (UV) radiation in sunlight. And a small number may be linked to an initial infection with a virus or bacteria.

Beyond those risk factors, some cancers are also inherited, meaning they are passed down through your family. According to the American Cancer Society, about 5 percent to 10 percent of all cancers are inherited from gene defects (mutations).

In some cases, researchers have figured out the exact genes that may cause cancer, and they can sometimes provide genetic counseling to help you understand your risk. But other cancers are caused by mutations that happen to an individual over time.

An important way for you to possibly detect cancer early, when it's easier to treat, is to undergo a cancer screening. Through screenings, doctors check people who don't necessarily have any cancer symptoms. Depending on your age, gender or other risk factors, your care team may recommend you get checked for certain cancers.

How do you know whether you're a good candidate for a cancer screening? You may need to get screened for certain types of cancer if you:

Have had cancer before

Have a family member who's been diagnosed with cancer

Have used tobacco or worked with certain chemicals

Have a certain gene mutation linked to cancer

Have had a blood clot develop without a known reason

Are older

What is a cancer stage, and what does it mean?

Your doctor will likely describe your cancer by referencing its stage. Your cancer's stage can tell you and your care team a lot about your disease, including:

Severity of the cancer

Appropriate treatments, including any clinical trial options

Likelihood of recovery after treatment

Chances of the cancer returning (recurrence)

Your care team may need to conduct certain tests-such as a computed tomography (CT) scan or a biopsy-to determine your cancer stage.

Not all cancers are classified with the same staging system. However, the one most commonly used includes the following stages:

Stage 0: Cancer cells remain in the same place where they started. This may also be called cancer in situ, meaning that it hasn't grown or spread.

Stage 1: Cancer hasn't grown into nearby tissues or lymph nodes.

Stage 2: Cancer has grown into nearby tissues and possibly nearby lymph nodes.

Stage 3: Cancer has grown deeper into nearby tissues and may have spread to nearby lymph nodes, but not to distant parts of the body.

Stage 4: Cancer has spread to other parts of the body, or other organs. This is also called metastatic, or advanced, cancer.

Some cancers may also be described using a grade, which describes how different cancerous cells look under a microscope compared with healthy cells. Cells in a low-grade tumor don't look much different from healthy cells, while cells in a high-grade tumor look very different and may grow and spread more quickly.

How is cancer treated?

Treatment options depend on the type of cancer, its stage, if the cancer has spread and your general health. The goal of treatment is to kill as many cancerous cells while reducing damage to normal cells nearby. Advances in technology make this possible.

The three main treatments are:

The same cancer type in one individual is very different from that cancer in another individual. Within a single type of cancer, such as breast cancer, researchers are discovering subtypes that each requires a different treatment approach.

What is oncology?

The branch of medicine dedicated to diagnosing, treating and researching cancer is known as oncology, while a physician who works in the field is called an oncologist. Some oncologists focus solely on particular cancer types or treatments. Depending on the type, stage and location of a cancer, multiple oncology specialists may be involved in a patient's care. The field of oncology has three main specialties-medical, surgical and radiation-and numerous sub-specialties.

A medical oncologist is a licensed physician (typically in internal medicine) trained in diagnosing, staging and treating cancer. This specialist also leads the development of the cancer patient's treatment plan, which may include surgery, chemotherapy, immunotherapy, targeted therapy or hormone therapy, while also coordinating with other oncology specialists and clinicians who may have a role in the patient's care. A medical oncologist is also the doctor a cancer patient will continue to see after treatment, for checkups over the long-term.

A surgical oncologist is a surgeon who specializes in performing biopsies and removing cancerous tumors and surrounding tissue, as well as other cancer-related operations.

A radiation oncologist specializes in treating cancer with radiation therapy to shrink or destroy cancer cells or to ease cancer-related symptoms.

Many cancer types are treated by an oncology sub-specialty. Gynecologic oncologists, for example, are trained to treat cancers of the female reproductive system such as those affecting the uterus, cervix, or ovaries, while hematologic oncologists specialize in diagnosing and treating blood cancers (leukemia, lymphoma and multiple myeloma). A neuro-oncologist treats cancers of the brain, spine and peripheral nerves.

What can you do to manage the side effects of cancer treatment?

Supportive care services describe a broad range of therapies designed to combat side effects and maintain well-being. Treating cancer requires focusing on more than the disease alone; it must also address the pain, fatigue, depression and other side effects that come with it.

Supportive care services include:

What does the future hold for cancer treatment?

The future of cancer treatment lies in providing patients with an even greater level of personalization. Doctors are beginning to offer treatment options based on the genetic changes occurring in a specific tumor.

An innovative new diagnostic tool, the genomic tumor assessment, examines a patient's tumor genetically to identify the mechanism that caused the cancer. Genomic tumor assessment may result in a more personalized approach to cancer treatment.

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What is Cancer, Is it Common & How Do You Get It

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Cancer is the uncontrolled growth of abnormal cells and it starts when the body's normal control mechanism stops working. Get answers to common questions.

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This picture shows each of the checkpoints of the cell cycle, and it includes a description on the side of what goes on at each checkpoint.

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In this Amoeba Sisters video, they give a whole bunch of information about mitosis with entertaining and easy-to-understand visuals.

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Mitosis: The Amazing Cell Process that Uses Division to Multiply! (Updated)

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This website explains the two major forms of reproduction: sexual and asexual.

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Sexual reproduction

Process of creating new individual using two parent organisms

Asexual reproduction

Process of creating new individual using one parent organism

Offspring

New organism that results from reproduction

Gamete

Sex cell (in males: sperm; in females: eggs)

Fertilization

The joining of gametes to form a new organism

Zygote

Cell formed during the fusion of two gametes

Types of reproduction

There are two major forms of reproduction: sexual and asexual.

Sexual reproduction

Sexual reproduction requires two parents. Each parent contributes a gamete - a sex cell that has half of the normal DNA of a regular body cell. In males, the gametes are sperm and in females, the gametes are eggs.

When these two gamete combine during fertilization, the result is a zygote, which then continues to develop into an embryo.

Asexual reproduction

Asexual reproduction requires only one parent.

There are many types of asexual reproduction. Four major types are:

1) Binary fission: Single parent cell doubles its DNA, then divides into two cells. Usually occurs in bacteria.

2) Budding: Small growth on surface of parent breaks off, resulting in the formation of two individuals. Occurs in yeast and some animals (like the hydra below).

3) Fragmentation: Organisms break into two or more fragments that develop into a new individual. Occurs in many plants, as well as some animals (like coral, sponges, and starfish).

4) Parthenogenesis: An embryo develops from an unfertilized cell. Occurs in invertebrates, as well as in some fish, amphibians, and reptiles.

Comparing sexual vs asexual reproduction

Requires 2 parents

Requires 1 parent

Sperm fertilizes egg

Single organism makes an exact copy of itself

Used by animals, flowering plants, some fungi

Bacteria, some plants and fungi, few animals (sponges)

Offspring are different from parents

Offspring are identical to parent

Provides genetic variation, but time-consuming

Fast and easy, but no genetic variation

Common mistakes and misconceptions

Sexual reproduction is not necessarily "better" than asexual reproduction, or vice versa. If one type of reproduction was clearly advantageous over the other, we would see all organisms reproducing in that manner. However, both types of reproduction still exist in various organisms, telling us that each type of reproduction carries some kind of evolutionary advantage.

For example, sexual reproduction allows for variation, but gestation usually takes a long time and it requires heavy parental input. Asexual reproduction occurs quickly, but because all of the offspring have the same genetic information, individuals are more susceptible to disease.

Budding and fragmentation are not the same thing. Although they do appear similar, in fragmentation, the parent body breaks into distinct fragments and each fragment develops into a new individual or offspring. In budding, there must be an outgrowth (bud) that develops on the parent.

Some organisms are able to do both sexual and asexual reproduction. This is particularly true for fungi and plants (and rarely, animals - as in parthenogenesis). Often, the type of reproduction that they undergo depends on their environmental conditions or the point in their growth cycles.

Although sexual reproduction requires two parents, they do not always have to be two separate individuals. This may sound confusing, but some organisms are hermaphroditic, meaning they contain both male and female gametes. In this instance, those organisms are able to self-fertilize. Despite the fact that these gametes come from the same individual, we still consider this sexual reproduction, as two gametes are involved.

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Types of reproduction review (article) | Khan Academy

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Learn for free about math, art, computer programming, economics, physics, chemistry, biology, medicine, finance, history, and more. Khan Academy is a nonprofit with the mission of providing a free, world-class education for anyone, anywhere.

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This website describes what happens in the phases of Meiosis I and II, how it mix-and-matches genes, and provides an extra video to understand how meiosis can contribute to evolution and helps populations survive.

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Introduction

Mitosis is used for almost all of your body's cell division needs. It adds new cells during development and replaces old and worn-out cells throughout your life. The goal of mitosis is to produce daughter cells that are genetically identical to their mothers, with not a single chromosome more or less.

Meiosis, on the other hand, is used for just one purpose in the human body: the production of gametes -sex cells, or sperm and eggs. Its goal is to make daughter cells with exactly half as many chromosomes as the starting cell.

To put that another way, meiosis in humans is a division process that takes us from a diploid cell-one with two sets of chromosomes-to haploid cells-ones with a single set of chromosomes. In humans, the haploid cells made in meiosis are sperm and eggs. When a sperm and an egg join in fertilization, the two haploid sets of chromosomes form a complete diploid set: a new genome.

Phases of meiosis

In many ways, meiosis is a lot like mitosis. The cell goes through similar stages and uses similar strategies to organize and separate chromosomes. In meiosis, however, the cell has a more complex task. It still needs to separate sister chromatids (the two halves of a duplicated chromosome), as in mitosis. But it must also separate homologous chromosomes, the similar but nonidentical chromosome pairs an organism receives from its two parents.

These goals are accomplished in meiosis using a two-step division process. Homologue pairs separate during a first round of cell division, called meiosis I. Sister chromatids separate during a second round, called meiosis II.

Since cell division occurs twice during meiosis, one starting cell can produce four gametes (eggs or sperm). In each round of division, cells go through four stages: prophase, metaphase, anaphase, and telophase.

During prophase I, differences from mitosis begin to appear. As in mitosis, the chromosomes begin to condense, but in meiosis I, they also pair up. Each chromosome carefully aligns with its homologue partner so that the two match up at corresponding positions along their full length.

For instance, in the image below, the letters A, B, and C represent genes found at particular spots on the chromosome, with capital and lowercase letters for different forms, or alleles, of each gene. The DNA is broken at the same spot on each homologue-here, between genes B and C-and reconnected in a criss-cross pattern so that the homologues exchange part of their DNA.

This process, in which homologous chromosomes trade parts, is called crossing over. It's helped along by a protein structure called the synaptonemal complex that holds the homologues together. The chromosomes would actually be positioned one on top of the other-as in the image below-throughout crossing over; they're only shown side-by-side in the image above so that it's easier to see the exchange of genetic material.

You can see crossovers under a microscope as chiasmata, cross-shaped structures where homologues are linked together. Chiasmata keep the homologues connected to each other after the synaptonemal complex breaks down, so each homologous pair needs at least one. It's common for multiple crossovers (up to !) to take place for each homologue pair .

The spots where crossovers happen are more or less random, leading to the formation of new, "remixed" chromosomes with unique combinations of alleles.

After crossing over, the spindle begins to capture chromosomes and move them towards the center of the cell (metaphase plate). This may seem familiar from mitosis, but there is a twist. Each chromosome attaches to microtubules from just one pole of the spindle, and the two homologues of a pair bind to microtubules from opposite poles. So, during metaphase I, homologue pairs-not individual chromosomes-line up at the metaphase plate for separation.

When the homologous pairs line up at the metaphase plate, the orientation of each pair is random. For instance, in the diagram above, the pink version of the big chromosome and the purple version of the little chromosome happen to be positioned towards the same pole and go into the same cell. But the orientation could have equally well been flipped, so that both purple chromosomes went into the cell together. This allows for the formation of gametes with different sets of homologues.

In anaphase I, the homologues are pulled apart and move apart to opposite ends of the cell. The sister chromatids of each chromosome, however, remain attached to one another and don't come apart.

Finally, in telophase I, the chromosomes arrive at opposite poles of the cell. In some organisms, the nuclear membrane re-forms and the chromosomes decondense, although in others, this step is skipped-since cells will soon go through another round of division, meiosis II. Cytokinesis usually occurs at the same time as telophase I, forming two haploid daughter cells.

Cells move from meiosis I to meiosis II without copying their DNA. Meiosis II is a shorter and simpler process than meiosis I, and you may find it helpful to think of meiosis II as "mitosis for haploid cells."

The cells that enter meiosis II are the ones made in meiosis I. These cells are haploid-have just one chromosome from each homologue pair-but their chromosomes still consist of two sister chromatids. In meiosis II, the sister chromatids separate, making haploid cells with non-duplicated chromosomes.

During prophase II, chromosomes condense and the nuclear envelope breaks down, if needed. The centrosomes move apart, the spindle forms between them, and the spindle microtubules begin to capture chromosomes.

The two sister chromatids of each chromosome are captured by microtubules from opposite spindle poles. In metaphase II, the chromosomes line up individually along the metaphase plate. In anaphase II, the sister chromatids separate and are pulled towards opposite poles of the cell.

In telophase II, nuclear membranes form around each set of chromosomes, and the chromosomes decondense. Cytokinesis splits the chromosome sets into new cells, forming the final products of meiosis: four haploid cells in which each chromosome has just one chromatid. In humans, the products of meiosis are sperm or egg cells.

How meiosis "mixes and matches" genes

The gametes produced in meiosis are all haploid, but they're not genetically identical. For example, take a look the meiosis II diagram above, which shows the products of meiosis for a cell with chromosomes. Each gamete has a unique "sample" of the genetic material present in the starting cell.

As it turns out, there are many more potential gamete types than just the four shown in the diagram, even for a cell with only four chromosomes. The two main reasons we can get many genetically different gametes are:

Crossing over. The points where homologues cross over and exchange genetic material are chosen more or less at random, and they will be different in each cell that goes through meiosis. If meiosis happens many times, as in humans, crossovers will happen at many different points.

Random orientation of homologue pairs. The random orientation of homologue pairs in metaphase I allows for the production of gametes with many different assortments of homologous chromosomes.

When we layer crossing over on top of this, the number of genetically different gametes that you-or any other person-can make is effectively infinite.

Check out the video on variation in a species to learn how genetic diversity generated by meiosis (and fertilization) is important in evolution and helps populations survive.

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Meiosis | Cell division | Biology (article) | Khan Academy

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Learn for free about math, art, computer programming, economics, physics, chemistry, biology, medicine, finance, history, and more. Khan Academy is a nonprofit with the mission of providing a free, world-class education for anyone, anywhere.

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This diagram compares and contrasts sexual and asexual reproduction.

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This diagram shows how cancer cells are able to spread and multiply.

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This brief video goes over how cancer starts and spreads in a cell, and provides additional statistics about the disease.

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This article by Khan Academy goes over mitosis and its phases.

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Introduction

What do your intestines, the yeast in bread dough, and a developing frog all have in common? Among other things, they all have cells that carry out mitosis, dividing to produce more cells that are genetically identical to themselves.

Why do these very different organisms and tissues all need mitosis? Intestinal cells have to be replaced as they wear out; yeast cells need to reproduce to keep their population growing; and a tadpole must make new cells as it grows bigger and more complex.

What is mitosis?

Mitosis is a type of cell division in which one cell (the mother) divides to produce two new cells (the daughters) that are genetically identical to itself. In the context of the cell cycle, mitosis is the part of the division process in which the DNA of the cell's nucleus is split into two equal sets of chromosomes.

The great majority of the cell divisions that happen in your body involve mitosis. During development and growth, mitosis populates an organism's body with cells, and throughout an organism's life, it replaces old, worn-out cells with new ones. For single-celled eukaryotes like yeast, mitotic divisions are actually a form of reproduction, adding new individuals to the population.

In all of these cases, the "goal" of mitosis is to make sure that each daughter cell gets a perfect, full set of chromosomes. Cells with too few or too many chromosomes usually don't function well: they may not survive, or they may even cause cancer. So, when cells undergo mitosis, they don't just divide their DNA at random and toss it into piles for the two daughter cells. Instead, they split up their duplicated chromosomes in a carefully organized series of steps.

Phases of mitosis

Mitosis consists of four basic phases: prophase, metaphase, anaphase, and telophase. Some textbooks list five, breaking prophase into an early phase (called prophase) and a late phase (called prometaphase). These phases occur in strict sequential order, and cytokinesis - the process of dividing the cell contents to make two new cells - starts in anaphase or telophase.

You can remember the order of the phases with the famous mnemonic: [ Please] Pee on the MAT. But don't get too hung up on names - what's most important to understand is what's happening at each stage, and why it's important for the division of the chromosomes.

Let's start by looking at a cell right before it begins mitosis. This cell is in interphase (late G phase) and has already copied its DNA, so the chromosomes in the nucleus each consist of two connected copies, called sister chromatids. You can't see the chromosomes very clearly at this point, because they are still in their long, stringy, decondensed form.

This animal cell has also made a copy of its centrosome, an organelle that will play a key role in orchestrating mitosis, so there are two centrosomes. (Plant cells generally don't have centrosomes with centrioles, but have a different type of microtubule organizing center that plays a similar role.)

In late prophase (sometimes also called prometaphase), the mitotic spindle begins to capture and organize the chromosomes.

The chromosomes become even more condensed, so they are very compact.

The nuclear envelope breaks down, releasing the chromosomes.

The mitotic spindle grows more, and some of the microtubules start to "capture" chromosomes.

Microtubules can bind to chromosomes at the kinetochore, a patch of protein found on the centromere of each sister chromatid. ( Centromeres are the regions of DNA where the sister chromatids are most tightly connected.)

Microtubules that bind a chromosome are called kinetochore microtubules. Microtubules that don't bind to kinetochores can grab on to microtubules from the opposite pole, stabilizing the spindle. More microtubules extend from each centrosome towards the edge of the cell, forming a structure called the aster.

Cytokinesis, the division of the cytoplasm to form two new cells, overlaps with the final stages of mitosis. It may start in either anaphase or telophase, depending on the cell, and finishes shortly after telophase.

In animal cells, cytokinesis is contractile, pinching the cell in two like a coin purse with a drawstring. The "drawstring" is a band of filaments made of a protein called actin, and the pinch crease is known as the cleavage furrow. Plant cells can't be divided like this because they have a cell wall and are too stiff. Instead, a structure called the cell plate forms down the middle of the cell, splitting it into two daughter cells separated by a new wall.

When cytokinesis finishes, we end up with two new cells, each with a complete set of chromosomes identical to those of the mother cell. The daughter cells can now begin their own cellular "lives," and - depending on what they decide to be when they grow up - may undergo mitosis themselves, repeating the cycle.

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Phases of mitosis | Mitosis | Biology (article) | Khan Academy

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Learn for free about math, art, computer programming, economics, physics, chemistry, biology, medicine, finance, history, and more. Khan Academy is a nonprofit with the mission of providing a free, world-class education for anyone, anywhere.

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This diagram shows what happens to the cells in each phase of mitosis.

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This diagram shows what happens to cells in each phase of meiosis I and meiosis II.

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This fun Amoeba Sisters video thoroughly explains what happens to cells that undergo meiosis, and also provides additional information about the matter.