cell division essay titles

Biology: Mitosis, or Cell Division

How it works

Mitosis, or Cell division, happens (or occurs) when a cell goes through multiple stages, known as the cell cycle, and as the cell goes though each stage, the cell eventually divides and produces two identical daughter cells.

The main purpose of Mitosis (or Cell division) is to produce and grow cells that make the human body function properly. This organized process is highly essential for replacing old and worn out cells, tissue growth, development, and extremely important for tissue repair and loss of tissue caused by factors, such as diseases.

As mentioned earlier, the cell cycle is basically a series of stages, in which somatic cells go through and a replication of the somatic cell is produced. Additionally, the cell cycle has two basic and major phases (or stages) known as Interphase and Mitotic (M) phase. It also has an additional stage known as Cytokinesis.

Interphase is the stage where cells prepare themselves for cell division. There are three distinctive phases (stages) within the Interphase stage of the cell cycle. These three stages are known as G1, S, and G2. The G1 phase, also called the first gap stage, is where cells grow and produce more organelles, more proteins, and new structures required for the replication of DNA. Once all that happens, the somatic cells then go into the S phase. The S phase, also called synthesis, is where DNA is replicated. It starts off with 46 chromosomes (pieces of DNA) and ends up with 92 sister chromatids (identical pieces of DNA held together by a centromere). And finally, the last stage of Interphase is the G2 phase. The G2 phase, also called the second gap stage, is rather quicker than the other stages within the cell cycle.

During the G2 phase, cells continue to grow and make final preparations for mitosis (cell division). After Interphase, the cells then go through the Mitotic (M) phase of the cell cycle. According to the book, Anatomy and Physiology: An Integrative Approach, it states that, “Two distinct events occur in this phase to produce two new cells: Mitosis, which is division of the nucleus, and cytokinesis, which is the division of the cytoplasm. Mitosis begins first with cytokinesis starting and overlapping with later stages of mitosis” (McKinley 144).

To add on, the Mitotic (M) phase also has three distinctive stages called: Prophase, Metaphase, Anaphase, and Telophase. The first stage of mitosis is Prophase. During prophase, chromatin starts to condense and coil into chromosomes. Mitotic spindle fibers start to form from the centrioles. Centrioles will then pull apart and separate to opposite ends of the cell. At the end of prophase, the chromosomes finish condensing and become very visible and both the nuclear envelope and nucleolus break down and disappear. The second stage of mitosis is Metaphase.

During this stage, spindle fibers begin to connect to chromosomes at the centromere and the chromosomes will then line up in a straight line on the metaphase plate region of the cell. The third stage of mitosis is Anaphase. In the article, Mitosis, the writer J. Richard McIntosh, describes anaphase as, “the separation of each chromosome into two identical parts, followed by their movement toward the opposite ends of the cell.” In other words, the “glue” holding the sister chromatids together breaks down and chromosomes of each pair are separated and then pulled towards the opposite ends of the cell. The fourth stage of mitosis is Telophase.

Here chromosomes begin to decondense and return to stringy form of chromatin, a nucleolus reforms from each new nucleus from two individual cells,  the mitotic spindle fibers will break up and disappear,  and finally new nuclear envelopes form around each pair of chromosomes. Lastly, Cytokinesis is the last and final event of mitosis. Cytokinesis, as mentioned earlier, is the division of the cytoplasm and it begins during late anaphase and continues through telophase. When cleavage furrow appears during cytokinesis, usually that points where the cytoplasm is being divided and two new daughter cells are formed, which then results in the completion of mitosis (cell division).

Tochtli, the main character and narrator in the novel, in my opinion is a static character. Tochtli does not go through a dramatic change in the book; yes, he cried towards the end of the book, but that isn’t a dramatic change of character. The reason why I think Tochtli is a static character is because he was basically the same person (character) throughout the novel. He was a young boy who was demanding and absorbing violence. While explaining how solidarity his family’s “gang” is and how his father, Yolcaut, buys him hats, Tochtli states, “Although now more than new hats what I want is a Liberian pygmy hippopotamus. I’ve already written it down on the list of things I want and given it to Miztli” (Villalobos 5).

Here it supports why Tochtli is demanding throughout the book because Tochtli is that one kid who asks for things because he feels like it. Yes, he is a young child and young children do tend to ask for things when it’s unnecessary, but throughout the book Tochtli is consistent when asking his father for new things. For example, Tochtli’s number one wish was to get a Liberian pygmy hippopotamus and he gets mad or should I say “mute” when his father keeps telling him that he’ll get it for him later, which he ultimately does. Not to mention, towards the end of the book he wants a Samurai sword, but he knows that his father wouldn’t allow him to have a Samurai sword, so he secretly tells Miztli to get him a Samurai sword.

Another reason why Tochtli is a static character is because he is into violence. There are scenes where Tochtli is continuously seeing violence on television which causes him to absorb the violence going on around him and his town. Tochtli mentions, “Since then there’ve been corpses on the TV every day” (Villalobos 23).

Tochtli does not know better, but to believe what he sees on tv. Even before he sees all the violence going on from his own tv, he was already fantasized by the French and how the French used to cut off people’s heads with a guillotine. Not to mention, he also sees violence in his own home. There were scenes where Tochtli sees a man getting viciously beat by the palace guards and he also sees dead people getting eaten by his pets (two tigers and one lion).

There’s also another scene where Tochtli displays his absorption of violence. He was playing around with a gun and he ends up shooting and killing a lovebird. His first initial reaction was throwing the gun away because he didn’t know what was going to happen afterwards. This was basically his very first act of violence towards a living thing and he acted totally normal and he seem not to care at all.

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7.2: Cell Cycle and Cell Division

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• Page ID 16754

• Suzanne Wakim & Mandeep Grewal
• Butte College

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So Many Cells!

The baby in Figure \(\PageIndex{1}\) has a lot of growing to do before they are as big as their mom. Most of their growth will be the result of cell division. By the time the baby is an adult, their body will consist of trillions of cells. Cell division is just one of the stages that all cells go through during their life. This includes cells that are harmful, such as cancer cells. Cancer cells divide more often than normal cells and grow out of control. In fact, this is how cancer cells cause illness. In this concept, you will read about how cells divide, what other stages cells go through, and what causes cancer cells to divide out of control and harm the body.

The Cell Cycle

Cell division is the process in which one cell, called the parent cell, divides to form two new cells, referred to as daughter cells. How this happens depends on whether the cell is prokaryotic or eukaryotic. Cell division is simpler in prokaryotes than eukaryotes because prokaryotic cells themselves are simpler. Prokaryotic cells have a single circular chromosome, no nucleus, and few other organelles. Eukaryotic cells, in contrast, have multiple chromosomes contained within a nucleus and many other organelles. All of these cell parts must be duplicated and then separated when the cell divides. Cell division is just one of several stages that a cell goes through during its lifetime. The cell cycle is a repeating series of events that include growth, DNA synthesis, and cell division. The cell cycle in prokaryotes is quite simple: the cell grows, its DNA replicates, and the cell divides. This form of division in prokaryotes is called asexual reproduction. In eukaryotes, the cell cycle is more complicated.

Eukaryotic Cell Cycle

Figure \(\PageIndex{2}\) represents the cell cycle of a eukaryotic cell. As you can see, the eukaryotic cell cycle has several phases. The mitotic phase (M) includes both mitosis and cytokinesis. This is when the nucleus and then the cytoplasm divide. The other three phases (G 1 , S, and G 2 ) are generally grouped together as interphase . During interphase, the cell grows, performs routine life processes, and prepares to divide. These phases are discussed below.

The Interphase of the eukaryotic cell cycle can be subdivided into the following phases (Figure \(\PageIndex{2}\)).

• Growth Phase 1 (G 1 ): The cell spends most of its life in the first gap (sometimes referred to as growth) phase, G 1 . During this phase, a cell undergoes rapid growth and performs its routine functions. During this phase, the biosynthetic and metabolic activities of the cell occur at a high rate. The synthesis of amino acids and hundreds of thousands or millions of proteins that are required by the cell occurs during this phase. Proteins produced include those needed for DNA replication. If a cell is not dividing, the cell enters the G 0 phase from this phase.
• G 0 phase: The G 0 phase is a resting phase where the cell has left the cycle and has stopped dividing. Non-dividing cells in multicellular eukaryotic organisms enter G 0 from G 1 . These cells may remain in G 0 for long periods of time, even indefinitely, such as with neurons. Cells that are completely differentiated may also enter G 0 . Some cells stop dividing when issues of sustainability or viability of their daughter cells arise, such as with DNA damage or degradation, a process called cellular senescence . Cellular senescence occurs when normal diploid cells lose the ability to divide, normally after about 50 cell divisions.
• Synthesis Phase (S): Dividing cells enter the Synthesis (S) phase from G 1 . For two genetically identical daughter cells to be formed, the cell’s DNA must be copied through DNA replication. When the DNA is replicated, both strands of the double helix are used as templates to produce two new complementary strands. These new strands then hydrogen bond to the template strands and two double helices form. During this phase, the amount of DNA in the cell has effectively doubled, though the cell remains in a diploid state.
• Growth Phase 2 (G 2 ): The second gap (growth) (G 2 ) phase is a shortened growth period in which many organelles are reproduced or manufactured. Parts necessary for mitosis and cell division are made during G 2 , including microtubules used in the mitotic spindle.

Mitotic Phase

Before a eukaryotic cell divides, all the DNA in the cell’s multiple chromosomes is replicated. Its organelles are also duplicated. This happens in the interphase. Then, when the cell divides (mitotic phase), it occurs in two major steps, called mitosis and cytokinesis , both of which are described in greater detail in the concept Mitotic Phase: Mitosis and Cytokinesis .

• The first step in the mitotic phase of a eukaryotic cell is mitosis, a multi-phase process in which the nucleus of the cell divides. During mitosis, the nuclear envelope (membrane) breaks down and later reforms. The chromosomes are also sorted and separated to ensure that each daughter cell receives a complete set of chromosomes.
• The second major step is cytokinesis. This step, which occurs in prokaryotic cells as well, is when the cytoplasm divides and two daughter cells form.

Control of the Cell Cycle

If the cell cycle occurred without regulation, cells might go from one phase to the next before they were ready. What controls the cell cycle? How does the cell know when to grow, synthesize DNA, and divide? The cell cycle is controlled mainly by regulatory proteins. These proteins control the cycle by signaling the cell to either start or delay the next phase of the cycle. They ensure that the cell completes the previous phase before moving on. Regulatory proteins control the cell cycle at key checkpoints, which are shown in Figure \(\PageIndex{3}\). There are a number of main checkpoints:

• The G1 checkpoint: just before entry into the S phase, makes the key decision of whether the cell big enough to divide. If the cell is not big enough, it goes into the resting period (G 0 )
• DNA synthesis Checkpoint: The S checkpoint determines if the DNA has been replicated properly.
• The mitosis checkpoint: This checkpoint ensures that all the chromosomes are properly aligned before the cell is allowed to divide.

Cancer and the Cell Cycle

Cancer is a disease that occurs when the cell cycle is no longer regulated. This happens because a cell’s DNA becomes damaged. This results in mutations in the genes that regulate the cell cycle. Damage can occur due to exposure to hazards such as radiation or toxic chemicals. Cancerous cells generally divide much faster than normal cells. They may form a mass of abnormal cells called a tumor (see Figure \(\PageIndex{4}\)). The rapidly dividing cells take up nutrients and space that normal cells need. This can damage tissues and organs and eventually lead to death. When uncontrolled cell division happens in the bone marrow, abnormal and nonfunctional blood cells are produced because the division is happening before the cell is ready for division. In these types of cancer, there is not any evident tumor.

Feature: Human Biology in the News

Henrietta Lacks sought treatment for her cancer at Johns Hopkins University Hospital at a time when researchers were trying to grow human cells in the lab for medical testing. Despite many attempts, the cells always died before they had undergone many cell divisions. Mrs. Lacks's doctor took a small sample of cells from her tumor without her knowledge and gave them to a Johns Hopkins researcher, who tried to grow them on a culture plate. For the first time in history, human cells grown on a culture plate kept dividing...and dividing and dividing and dividing. Copies of Henrietta's Lacks cells — called HeLa cells for her name — are still alive today. In fact, there are currently many billions of HeLa cells in laboratories around the world!

Why Henrietta Lacks' cells lived on when other human cells did not is still something of a mystery, but they are clearly extremely hardy and resilient cells. By 1953, when researchers learned of their ability to keep dividing indefinitely, factories were set up to start producing the cells commercially on a large scale for medical research. Since then, HeLa cells have been used in thousands of studies and have made possible hundreds of medical advances. For example, Jonas Salk used the cells in the early 1950s to test his polio vaccine. Over the decades since then, HeLa cells have been used to make important discoveries in the study of cancer, AIDS, and many other diseases. The cells were even sent to space on early space missions to learn how human cells respond to zero gravity. HeLa cells were also the first human cells ever cloned, and their genes were some of the first ever mapped. It is almost impossible to overestimate the profound importance of HeLa cells to human biology and medicine.

You would think that Henrietta Lacks' name would be well known in medical history for her unparalleled contributions to biomedical research. However, until 2010, her story was virtually unknown. That year, a science writer named Rebecca Skloot published a nonfiction book about Henrietta Lacks, named The Immortal Life of Henrietta Lacks. Based on a decade of research, the book is riveting, and it became an almost instantaneous best seller. As of 2016, Oprah Winfrey and collaborators planned to make a movie based on the book, and in recent years, numerous articles about Henrietta Lacks have appeared in the press.

Ironically, Henrietta herself never knew her cells had been taken, and neither did her family. While her cells were making a lot of money and building scientific careers, her children were living in poverty, too poor to afford medical insurance. The story of Henrietta Lacks and her immortal cells raises ethical issues about human tissues and who controls them in biomedical research. However, there is no question that Henrietta Lacks deserves far more recognition for her contribution to the advancement of science and medicine.

• What are the two main phases of the cell cycle in a eukaryotic cell?
• Describe the three phases of interphase in a eukaryotic cell.
• Explain how the cell cycle is controlled.
• How is cancer-related to the cell cycle?
• What are the two major steps of cell division in a eukaryotic cell?
• In which phase of the eukaryotic cell cycle do cells typically spend most of their lives?
• Which phases of the cell cycle will have cells with twice the amount of DNA? Explain your answer.
• If there is damage to a gene that encodes for a cell cycle regulatory protein, what do you think might happen? Explain your answer.
• True or False . Cells go into G 0 if they do not pass the G 1 checkpoint.
• Cytokinesis
• What were scientists trying to do when they took tumor cells from Henrietta Lacks? Why did they specifically use tumor cells to try to achieve their goal?

Explore More

The video below discusses the cell cycle and how it relates to cancer.

Attributions

• Woman holding baby by M.T ElGassier , via Unsplash license
• Cell cycle by Zephyris, CC BY-SA 3.0 Wikimedia Commons
• Cell cycle checkpoints by Lumen Learning, CC BY 4.0
• Colon cancer by Emmanuelm, CC BY 3.0 via Wikimedia Commons
• HeLa cells by National Institutes of Health (NIH), public domain via Wikimedia Commons
• Text adapted from Human Biology by CK-12 licensed CC BY-NC 3.0

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Unit 15: Cell division

About this unit.

This unit is part of the Biology library. Browse videos, articles, and exercises by topic.

Introduction to cell division

• Fertilization terminology: gametes, zygotes, haploid, diploid (Opens a modal)
• Zygote differentiating into somatic and germ cells (Opens a modal)
• Chromosomes, chromatids and chromatin (Opens a modal)
• Chromosomes (Opens a modal)
• Intro to cell division Get 3 of 4 questions to level up!

The cell cycle and mitosis

• Interphase (Opens a modal)
• Phases of the cell cycle (Opens a modal)
• Mitosis (Opens a modal)
• Phases of mitosis (Opens a modal)
• Bacterial binary fission (Opens a modal)
• Mitosis questions Get 3 of 4 questions to level up!
• Comparing mitosis and meiosis (Opens a modal)
• Chromosomal crossover in meiosis I (Opens a modal)
• Phases of meiosis I (Opens a modal)
• Phases of meiosis II (Opens a modal)
• Meiosis (Opens a modal)
• Sexual life cycles (Opens a modal)
• Meiosis Get 3 of 4 questions to level up!

Cell cycle regulation, cancer, and stem cells

• Cell cycle checkpoints (Opens a modal)
• Cell cycle regulators (Opens a modal)
• Cancer (Opens a modal)
• Cancer and the cell cycle (Opens a modal)
• Apoptosis (Opens a modal)
• Cell cycle regulation Get 3 of 4 questions to level up!
• Apoptosis Get 3 of 4 questions to level up!

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• v.366(1584); 2011 Dec 27

The cell cycle

1 Cancer Research UK, Clare Hall Laboratories, South Mimms, Herts EN6 3LD, UK

Kim Nasmyth

2 Oxford Centre for Integrative Systems Biology, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK

Béla Novák

‘Dividing cells pass through a regular sequence of cell growth and division, known as the cell cycle’, according to a college textbook of biology published in 1983 [ 1 ], 5 years before the underlying principles of control were first laid bare during 1988, the annus mirabilis of cell cycle research [ 2 , 3 ]. One of the key architects of that revolution, Paul Nurse, was elected as President of the Royal Society in 2010, and this volume is intended in part as a tribute and in part as a reflection of what we now know, and what remains still to be found out about cell proliferation. Lest we forget that cells have fates other than their own reproduction, Pat O'Farrell [ 4 ] reminds us that many cells in our bodies survive for long periods in a quiescent state. He considers quiescence from the perspective of the developmental biologist, and sees growth factors as surrogates for nutritional signals. He surveys the complexity and the richness of growth control in higher eukaryotes, rightly pointing out what an important topic for future research this remains. This problem is also attacked from the perspective of the single starving cell by Yanagidai, who have been recently studying the effects of nitrogen or glucose deprivation on fission yeast [ 5 ]. It turns out that the results are daunting. Wild-type yeast undergoes two rapid divisions to generate quasi-spherical cells if they are suddenly deprived of nitrogen, and undergoes startling changes in intracellular morphology and metabolism that remain difficult to comprehend. Interestingly, defects in these adaptions are accompanied by cell death and hundreds of different genes, in many distant pathways, are required to respond to starvation or to ‘wake up’ when better times come along.

Long-term survival, we must remind ourselves, requires not only cell division but also sex. Dan Mazia, who was the guru of cell division of the 1950s and 1960s, put it thus: ‘More often than not, questions beginning with ‘Why’ are inane and of no service in scientific discourse. In biology, they sometimes make sense. If we ask why cells must divide, the answer can be given in terms of what happens if they do not. The answer is that they die, no matter what criterion of death we apply’ [ 6 , pp. 82–83]. This applies to organisms as well as cells, of course, and it is still somewhat mysterious that we humans can all trace our ancestry back several billion years, yet we are all mortal. The continuity of the germ cells is something that successfully evolved, but is hard to explain and rarely examined. Yet, formation of gametes is amenable to genetic analysis, and van Werven & Amon [ 7 ] present an accessible and wide-ranging survey of the process in budding yeast, fission yeast and higher eukaryotes that makes clear what a delicately regulated process it is. Certain features seem to be common: the existence of a ‘master regulator’ whose activity depends critically on a very particular combination of nutritional or developmental signals, as well as downstream regulatory protein kinase cascades, in particular the TOR pathway and the cyclic AMP-dependent protein kinase. For some reason, functioning mitochondria are apparently also required for successful gamete formation in yeast and mice. Presumably, that has only been true since oxygen entered Earth's atmosphere two and a half billion years ago.

In ‘normal’ cell cycles, there is a gap between the end of mitosis and the start of DNA replication, and control of the G1 to S transition is an important point of no return in the cell cycle. Cross et al . [ 8 ] discuss the evolution of control networks at this stage of the cell cycle, comparing yeast with plants and animals. They find that many individual regulators have either undergone huge sequence divergence from the last common ancestor or have evolved from different origins. Despite this, the topology and dynamic properties of networks have striking similarities. Diffley [ 9 ] looks at the control of initiation of DNA replication and again notes the variety as well as the redundancy of mechanisms that ensure the genome is replicated once and only once each time a cell divides. Arguing from simple assumptions, he points out that suppression of re-replication must be close to 100 per cent efficiency and that a combination of mechanisms, each with a small but finite failure rate, is necessary to reduce the overall failure rate to acceptable levels.

High fidelity is also a major consideration for the control of key cell cycle transitions. The penalty for failure is high, the difference between success and failure is tiny, and mechanisms for assuring accuracy are numerous and robust. Having evolved over billions of years they may also be rather complicated and difficult to understand, as is the case with the so-called S-phase checkpoints, discussed in detail by Labib & De Piccoli [ 10 ]. As soon as people realized the importance of DNA and DNA replication for cells, in the early 1950s, they tested the effects of ionizing radiation and discovered that normal cells quickly stopped synthesizing DNA after X-ray damage (apart from very rare mutant individuals, who were extremely sensitive to X-irradiation and turned out—many years later—to carry mutations in the ATM protein kinase). These irradiated cells did not enter mitosis. After intense study, largely by geneticists, because biochemical analysis for such complex systems is for the most part too difficult, we are now aware of many if not most components of the S-phase checkpoint, but it is still difficult to appreciate how the system really works. Replication forks and collapsed replication forks are complicated structures and the details of how damage is sensed, signalled and repaired are complicated and only gradually being worked out in mechanistic detail. The virtue of Labib's account lies in its historical approach and his attention to describing the experiments that underlie our present understanding. Langerak & Russell [ 11 ] also discuss the effects of DNA damage on cell cycle progression and vice versa, concentrating on the mechanisms that repair double-strand breaks in DNA. These are largely twofold, non-homologous end joining (NHEJ), which tends to occur when DNA is broken during the G1 phase of the cell cycle, and homologous recombination (HR), a largely error-free repair process that uses sister chromatids to reconstruct lost DNA sequences. The latter requires production of long stretches of single-stranded DNA that search for neighbouring homologous DNA sequences and subsequently invade them. The abundance and the activity of a large cast of cofactors are regulated in such a way as to promote NHEJ during G1, when sister DNAs are absent, and HR during S and G2, when they are present.

A key issue in cell cycle studies has been the nature of the triggers for the onset of DNA replication and mitosis. Much to everyone's surprise, both turn out to be triggered by similar molecules, namely S- and M-phase-specific cyclin-dependent kinases (CDKs), and almost every article in this issue refers to these key cell cycle regulators. An important question about these enzymes, apart from their regulation, is their substrate specificity. In particular, and this was confusing in the early days of the modern era of cell cycle studies, how can it be that the same kinase initiates both S and M phase? Why, for example, do cells undergo DNA replication and not attempt to enter mitosis at the first appearance of CDK activity? Moreover, why do not cells re-replicate their chromosomes when a second rise in CDK activity triggers mitosis? Two explanations seemed possible at first: one was that different cyclins imbued Cdks with different properties, so S-phase cyclins promote S phase and M-phase cyclins catalyse mitosis. But an alternative, originally suggested by Paul Nurse and co-workers [ 12 ], is that it takes only a little Cdk activity to initiate S phase, but more to enter M phase. The available evidence suggests that the level of activity is indeed part of the story, as Uhlmann et al . [ 13 ] discuss in their article. However, this is only part of the story. Whether a cell enters to undergo DNA replication or mitosis in response to a rise in Cdk activity is as much determined by the presence or absence of substrates or structures for these kinases to work on. Thus, the reason why Cdks do not trigger S during G2 is that the pre-replication complexes required to initiate DNA replication are absent from this stage of the cell cycle. Likewise, G1 cells that have not yet replicated their DNA do not possess a pair of sister chromatids nor even the cohesion that will hold these together, and cannot undergo anything resembling a physiological mitosis until these have been produced.

Uhlmann et al . [ 13 ] take some trouble to examine whether ‘checkpoints’ impose order on the cell cycle, and conclude that, on the whole, they do not. We note, however, that the concept of checkpoint, while highly popular and therefore much abused in the literature, is often inappropriate in the context of the cell cycle as well as being rather fuzzy on close inspection. In an earlier generation, before yeast genetics was applied to cell cycle control, people like Dan Mazia used to talk about ‘Points of no return’ rather than ‘Checkpoints’. The idea of the checkpoint is that you may not proceed to the next process or event until the one in which you are presently engaged is complete: a quality control check. But there is something else as well—once you have finished a task and been allowed to pass on, you cannot go back. This applies equally to the G1–S, the G2–M and the metaphase to anaphase transitions. Uhlmann et al . [ 13 ] argue that even if the level of Cdks activity has an important role in determining entry into S or M, regulation of phosphatase activity plays an equally important part. The various thresholds for cell cycle transitions are set by ratios of kinase activity to phosphatase activity and not by kinase activity per se . This theme continues in the contribution from Domingo-Sasanes et al. [ 14 ], who restrict their discussion to the control of mitosis, but focus on the recently discovered role of greatwall kinase as a controller of protein phosphatases that both regulate and antagonize Cdks at the G2–M transition.

This brings us to the end of the cell cycle, or the beginning of the next, the metaphase to anaphase transition. Musacchio [ 15 ] entitles his piece ‘Spindle assembly checkpoint: the third decade’, inviting the query, what's taking you so long? The answer is that this is a very complicated piece of machinery involving both hardware (the kinetochore itself, and its connection with spindle microtubules) and software—the error correction mechanisms and surveillance mechanisms that constitute the spindle assembly checkpoint (SAC). Interestingly, this regulatory system, unlike other the so-called checkpoints, has little or no role in repairing the damage sensed and appears solely concerned with regulating cell cycle progression. At least three or four protein kinases (and presumably their counterpart phosphatases) are involved as well as specific regulatory proteins such as Mad2. Working out how the SAC functions will require greater understanding of kintetochore structure as well as further structural work on its target, the anaphase-promoting complex/cyclsome (APC/C). Nevertheless, it is clear that the structural approach has already been extremely illuminating. At the moment, it looks as if the mechanical basis for the tension sensor may be nothing more complicated than a substrate being pulled beyond the reach of a tethered kinase. We may hope that some of the other seemingly complex features of the mitotic checkpoint will proved to have a similarly simple basis, once we understand them.

David Barford's [ 16 ] magisterial review of the APC/C depends even more so on structural determination, but his recent impressive advances required him to work out ways of making large quantities of this enormous, complicated multi-subunit complex. As he describes, we can begin to see how the thing works, although mysteries still remain, particularly in its control. This is connected with the previous paper, of course, because somehow the SAC can reliably amplify a signal from a single kinetochore to inhibit millions of APC/Cs, and somehow (as anyone who has ever watched cells enter anaphase can testify) the inhibition is lifted when all the chromosomes are properly aligned on the metaphase plate, such that it looks as though someone fired a starting pistol ( figure 1 ) to signal chromosome separation.

Mazia's diagram of mitosis with the starting pistol (‘Trigger?’). Adapted from Mazia [ 6 ].

Pines & Hagan [ 17 ] revisit many of the points raised in the preceding articles from a wide-ranging perspective, but they go on to stress the importance of intensely local conditions controlling physically distant processes. A particular concern of theirs is the spindle pole in fission yeast and its role as the place where a commitment to mitosis is made first, and the centrosome in animal cells, which they argue plays a central role in the control of mitotic entry. They make a plea for more quantitative studies in cell biology, and urge the development of reporters that can monitor the local activity of protein kinases and phosphatases in living cells.

Hyman's article [ 18 ] takes up the same theme from a ‘systems biology’ perspective. Actually, one of his main concerns is people's understanding of exactly what is systems biology. Tony makes the important point that both time and space cover vast ranges of scale in biology. Molecular movements in proteins occur on the microsecond timescale, yet it takes years for a human to reach sexual maturity. Or look at Barford's beautiful pictures of the APC/C elsewhere in this issue and remind yourself that a human on the same scale would be roughly twice as big as the Earth. Hyman makes the same plea as Pines and Hagan: more emphasis on quantitative data is necessary to begin to make sense of biological models. He also provides a useful definition for systems biology: ‘It is the approach of collecting quantitative biological information at one level of complexity, and using it to build models that describe the next level of complexity’. Thus, he claims that ‘systems biology is an approach, not a field’. The more we learn about the complexity of the regulatory network controlling cell proliferation the more useful are the systems biology approaches in the cell cycle field.

The final contribution to this collection by Kronja & Orr-Weaver [ 19 ] covers one of the less familiar areas of cell cycle control, namely the control of expression of mRNA at the level of translation. It turns out that there is quite a lot to say, not only in the authors' favourite model system, the Drosophila egg, zygote and early embryo, but also in yeast, frogs and even human cells. It has been known for some time that translation of normal capped mRNAs declines during mitosis, whereas internal ribosome entry sites (IRES) are preferentially used, and some of the important examples of this switch have recently come to light; their underproduction causes faults in cytokinesis. The majority of well-established and better worked-out examples do come from eggs and early embryos, however, which is probably not surprising considering that transcriptional control of gene expression is largely absent in these (typically) enormous cells. The regulatory networks are quite complicated, as can be seen from figure 2 of this review. One suspects that there is rather a lot to be learned still in this area.

Altogether, this collection of articles provides a kind of partial snapshot of the current state of understanding in some of the most active areas of enquiry in the broad field of the cell cycle. For the most part, the general principles are reasonably well defined, but the precise details of molecular mechanism in many cases prove harder to pin down than perhaps one might have expected 25 years ago. Moreover, there remain considerable tracts of uncharted territory, that is, areas where even the basic principles are difficult to comprehend. First and foremost among these is the problem of the regulation and coordination of cell growth, and the relationship between growth control and division control, which was arguably the starting point when Paul Nurse decided to work on fission yeast with the late Murdoch Mitchison. It is perhaps appropriate to end with an acknowledgement of Murdoch's contribution to this field. Apart from definitively defining the field in the title of his 1971 monograph ‘The Biology of the Cell Cycle’ [ 20 ] (the term was not in common currency before this, surprisingly enough), Murdoch served as a stimulating, quizzical, generous mentor to Paul Nurse as well as two of the editors of this issue, Kim Nasmyth and Bela Novak. Murdoch took a keen interest in the cell cycle field until the very end, and his passing marks the end of an exciting and heroic era.

Cell Division: Mitosis and Meiosis

Introduction, meiosis and embryogenesis, recommendations for the patient.

Living multicellular organisms are fragile biological systems that have the potential to be damaged by negative factors. Thus, touching the edge of the blade on the skin surface usually causes injury to the epidermis’ soft tissues. Nevertheless, somatic cells, which form the basis of tissues, are protected with regeneration, which makes it possible to start the processes of cell division, including the repair of damage. Cell cloning, which results in the creation of identical cells, is called Mitosis. Another type of division, Meiosis, is aimed at forming germ ones: sperm cells and eggs. This essay discusses two processes in the context of a patient with wound healing problems and embryogenesis stages.

Mitosis is a fundamental process underlying the preservation of genetic diversity. First of all, among the diversity should be highlighted skin cells, as it is one of the few species of living structures that have direct contact with the environment. The skin consists of three layers: hypodermis, dermis, and epidermis — only the outer layer is traditionally damaged by light wounds. In the case of the patient, she has problems with wound healing, which indicates a disturbance of mitosis processes, as the central postulate of cell theory says that all cells are formed from cells.

Mitosis is a short but essential stage in the life cycle of cells, during which the division of the parent individual in two occurs. This model is typical for eukaryotic somatic cells with a diploid set of chromosomes — as in the epidermis. Mitosis includes four substations, each of which differs in the nature of the division (BiologyWeymouthHS, 2018). Thus, at the first stage of Mitosis, Prophase, there is the destruction of the nuclear shell in the cell, and the content of the nucleus, DNA filaments, tightly twisted. Only at this stage chromosomes can be detected in the light microscope, and it is also the longest stage of cell division. The second stage is called Metaphase, and during this stage, the spindle apparatus’ microtubules, which began to form in the prosthesis, line up the chromosome at the cell equator. All genetic material is placed strictly in the middle, and each chromatid in the chromosome is connected with protein tubes. The Anaphase stage comes when the chromosomes are torn in half by shortening the tubes’ length, which leads to a temporary increase in DNA molecules inside the cell. If DNA were 46 molecules in Metaphase, there would be 92 DNA molecules in Anaphase (Campbell, 2009). The chromatids that are left of the chromosomes diverge to the cell poles, and the phase of Telophase begins. During the fourth phase, the shell of already two nuclei is restored, the equatorial boundary is formed, which breaks the cell into two parts. Thus, one diploid somatic skin cell forms two new cells identical to the first. This is where the process of tissue regeneration, which often takes place in the skin, rests. It is essential to recognize that Mitosis is an incredibly useful type of cell division since it keeps the genetic material unchanged and has high speed and autonomy. However, it often happens that it is not the variability that causes cell death.

Meiosis in the human body is realized only in the germ cells that form sperm and eggs. Meiosis is more complicated than Mitosis because it consists of two consecutive divisions, including four phases. These are Prophase I, Metaphase I, Anaphase I, and Telophase I, as well as Prophase II, Metaphase II, Anaphase II, and Telophase II (Vidyasagar, 2018). In general, the stages are similar to mitotic division, except that there are complexes of homologous chromosomes at the equator during Metaphase I. This is due to the processes of replication, conjugation, and crossover of chromosomes. As a result, four daughter cells have unique genetic diversity in comparison with the original one. For this reason, Meiosis has a significant advantage — it creates the conditions for adaptation and survival of organisms. However, this type of division requires more time and energy. Meiosis products, male sperm, and female eggs are mixed during fertilization than the embryogenesis process begins.

Embryogenesis is developing a fetus within the mother or in a laboratory environment where, through several mitotic divisions and differentiation, a single-celled zygote becomes a complete child. Once the sex cells have merged into one, multiple mitotic divisions occur. Moreover, the cells at this stage do not increase in volume, and the final product, Morula, is proportional to the zygote. The inner cavity begins to form, resulting in Blastula. After that, one part of the cells hangs inward to form an inner layer, creating a two-layer embryo called Gastrula. At this stage, cell differentiation processes are activated, and the first embryo tissue appears. Finally, a complex structure is formed, the Neurula, in which three layers of cells are already present, and their functional division continues.

Naturally, it is impossible to change the processes taking place in the structures of living cells. In other words, the woman will not directly force the damaged somatic and sexual cells to divide normally. General recommendations may include maintaining a healthy lifestyle, eating healthy foods, and regular exercise, which may help to restore the energy balance of cells. There are some factors to stimulate Mitosis, the use of which will speed up skin regeneration processes. However, if the woman decides to take more courageous steps, she may seek help from In Vitro Fertilization specialists. This procedure involves artificial insemination and incubation of the embryo, after which the embryo is placed in the uterine cavity for further development.

BiologyWeymouthHS. (2018). Cell Division. Web.

Campbell, N. A. (2009). Essential biology with physiology . London, England: Pearson Education.

Vidyasagar, A. (2018). What is meiosis ? Web.

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A key step in cell division is the partitioning of the chromosomes into the newly created daughter cells. Errors in chromosome segregation can lead to cancer, infertility, and developmental disorders. Chromosome segregation, and the subsequent division of the cell, involves diverse cellular and ...

Keywords : microtubules, actin, forces, microscopy, mitosis, meiosis, spindles, abscission, contractile ring, cytokinesis, motor proteins

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Cancer and The Process of Cell Division

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Introduction, the cell cycle, cell division, cell growth, cancer treatment.

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Frumin AM, Nussbaum J, Esposito M. Functional asplenia: demonstration of splenic activity by bone marrow scan. Blood 1979;59 Suppl 1:26-32.

Book chapter, or an article within a book

Wyllie AH, Kerr JFR, Currie AR. Cell death: the significance of apoptosis. In: Bourne GH, Danielli JF, Jeon KW, editors. International review of cytology. London: Academic; 1980. p. 251-306.

OnlineFirst chapter in a series (without a volume designation but with a DOI)

Saito Y, Hyuga H. Rate equation approaches to amplification of enantiomeric excess and chiral symmetry breaking. Top Curr Chem. 2007. doi:10.1007/128_2006_108.

Complete book, authored

Blenkinsopp A, Paxton P. Symptoms in the pharmacy: a guide to the management of common illness. 3rd ed. Oxford: Blackwell Science; 1998.

Online document

Doe J. Title of subordinate document. In: The dictionary of substances and their effects. Royal Society of Chemistry. 1999. http://www.rsc.org/dose/title of subordinate document. Accessed 15 Jan 1999.

Online database

Healthwise Knowledgebase. US Pharmacopeia, Rockville. 1998. http://www.healthwise.org. Accessed 21 Sept 1998.

Supplementary material/private homepage

Doe J. Title of supplementary material. 2000. http://www.privatehomepage.com. Accessed 22 Feb 2000.

University site

Doe, J: Title of preprint. http://www.uni-heidelberg.de/mydata.html (1999). Accessed 25 Dec 1999.

Doe, J: Trivial HTTP, RFC2169. ftp://ftp.isi.edu/in-notes/rfc2169.txt (1999). Accessed 12 Nov 1999.

Organization site

ISSN International Centre: The ISSN register. http://www.issn.org (2006). Accessed 20 Feb 2007.

Dataset with persistent identifier

Zheng L-Y, Guo X-S, He B, Sun L-J, Peng Y, Dong S-S, et al. Genome data from sweet and grain sorghum (Sorghum bicolor). GigaScience Database. 2011. http://dx.doi.org/10.5524/100012 .

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