Why can't cell division happen the other way around?

Mitosis in eukaryotes happen in this order: DNA replicates and then the cell divides. Why doesn't it happen in reverse order (i.e., cell divides and then replicates the DNA)? I am talking about diploid cells. Why has evolution favoured the first way?

If you are thinking of a process like meiosis but followed by DNA duplication, the problem is that this would create daughter cells that do not have the same genome as the parent cell.

The diploid genome of a sexually reproducing species' cell has different alleles of the same locus. If the cell replicates itself by passing one chromatid to each daughter cell which then duplicate that to make a diploid genome, the resulting cells will not have the same DNA as the original one since each of the daughter cells will have inherited only one of the available alleles. They will then make an exact copy of the DNA they have inherited and become diploid but with a new genome, one that did not exist in their parent. This is not good since the cells of an organism need to have the same genome in order to function in the same way.

The biggest problem is this: if you have only one copy of the DNA how is it going to divide it between the two cells so that both have a complete copy?

Why can't cell division happen the other way around? - Biology

What you need to know.

  • Why is cell division important to organisms?
  • What happens in cell division?
  • What is cancer?

All living things are made of cells. The cell is the basic unit of living things.

Some living things like bacteria are only made up of one cell. Other living things like us are made up of lots and lots and lots of cells.

Making new cells

So why do living things make new cells?

Basically, an organism (living thing) needs to make new cells so that they can grow and repair damaged parts of themselves e.g. cuts, broken bones.

Cell division

The following table shows the sequence of events of cell division stage by stage.

You have probably heard about cancer but may not know that cancer is a disease of cells. It develops when normal cell division goes out of control. Unlike normal cells, cancer cells make too many new cells and they don’t die when they are supposed to. They can form a group of cells called a tumour which grows into and damages the healthy cells around them. This can makes a person very sick.

So why do healthy cells start to divide uncontrollably? It is all down to the DNA. You already know that DNA contains the genetic instructions for a living thing. Well if the DNA in a cell gets damaged these instructions get broken and a cell can start to behave in a strange way.

Usually cancer is a disease of old age. But there are some things that can damage the DNA in a cell and lead to cancer. Things like smoking, unhealthy diet, lack of exercise, overexposure to sun, infection with a certain viruses (HPV) can all increase our risk of cancer. It is important to stress that many causes of cancer are simply unknown.

Types of Cell Division

Prokaryotic Cell Division

Prokaryotes replicate through a type of cell division known as binary fission. Prokaryotes are simple organism, with only one membrane and no division internally. Thus, when a prokaryote divides, it simply replicates the DNA and splits in half. The process is a little more complicated than this, as DNA must first be unwound by special proteins. Although the DNA in prokaryotes usually exists in a ring, it can get quite tangled when it is being used by the cell. To copy the DNA efficiently, it must be stretched out. This also allows the two new rings of DNA created to be separated after they are produced. The two strands of DNA separate into two different sides of the prokaryote cell. The cell then gets longer, and divides in the middle. The process can be seen in the image below.

The DNA is the tangled line. The other components are labeled. Plasmids are small rings of DNA that also get copied during binary fission and can be picked up in the environment, from dead cells that break apart. These plasmids can then be further replicated. If a plasmid is beneficial, it will increase in a population. This is in part how antibiotic resistance in bacteria happens. The ribosomes are small protein structures that help produce proteins. They are also replicated so each cell can have enough to function.

Eukaryotic Cell Division: Mitosis

Eukaryotic organisms have membrane bound organelles and DNA that exists on chromosomes, which makes cell division harder. Eukaryotes must replicate their DNA, organelles, and cell mechanisms before dividing. Many of the organelles divide using a process that is essentially binary fission, leading scientist to believe that eukaryotes were formed by prokaryotes living inside of other prokaryotes.

After the DNA and organelles are replicated during interphase of the cell cycle, the eukaryote can begin the process of mitosis. The process begins during prophase, when the chromosomes condense. If mitosis proceeded without the chromosomes condensing, the DNA would become tangled and break. Eukaryotic DNA is associated with many proteins which can fold it into complex structures. As mitosis proceeds to metaphase the chromosomes are lined up in the middle of the cell. Each half of a chromosome, known as sister chromatids because they are replicated copies of each other, gets separated into each half of the cell as mitosis proceeds. At the end of mitosis, another process called cytokinesis divides the cell into two new daughter cells.

Eukaryotic Cell Division: Meiosis

In sexually reproducing animals, it is usually necessary to reduce the genetic information before fertilization. Some plants can exist with too many copies of the genetic code, but in most organisms it is highly detrimental to have too many copies. Humans with even one extra copy of one chromosome can experience detrimental changes to their body. To counteract this, sexually reproducing organisms undergo a type of cell division known as meiosis. As before mitosis, the DNA and organelles are replicated. The process of meiosis contains two different cell divisions, which happen back-to-back. The first meiosis, meiosis I, separates homologous chromosomes. The homologous chromosomes present in a cell represent the two alleles of each gene an organism has. These alleles are recombined and separated, so the resulting daughter cells have only one allele for each gene, and no homologous pairs of chromosomes. The second division, meiosis II, separated the two copies of DNA, much like in mitosis. The end result of meiosis in one cell is 4 cells, each with only one copy of the genome, which is half the normal number.

Organisms typically package these cells into gametes, which can travel into the environment to find other gametes. When two gametes of the right type meet, one will fertilize the other and produce a zygote. The zygote is a single cell that will undergo mitosis to produce the millions of cells necessary for a large organism. Thus, most eukaryotes use both mitosis and meiosis, but at different stages of their lifecycle.

What is Plant Cell Division

Plant cell division is the production of two daughter plant cells from a mother cell. Plant’s vegetative cell division occurs by mitosis and gametes are produced by meiosis. During the mitotic division of plant cells, they undergo usual M phase and cytokinesis begins after the late stages of the M phase. The cytokinesis is significantly different in plant cells due to the presence of a cell wall. Plant cells form a new cell wall in between the two cells. The new cell wall is identified as the cell plate.

The formation of the cell plate occurs in several stages. First, the phragmoplast is created by assembling the remnants from the mitotic spindle. It is an array of microtubules which supports and guides the formation of the cell plate. Secondly, vesicles transfer into the division plane. Phragmoplast serves as the track for the vesicles that are trafficking. The vesicles contain lipids, proteins and carbohydrates required by the formation of the cell plate. These vesicles are fashioned to form a tubular-vesicular network. Membrane tubules are transformed into the forming membrane sheet while the callose begins to deposit on it. Next, other cell wall components together with cellulose are deposited. Then, the excess membrane and other materials from the cell plate are recycled. The membrane tubules are widen to fuse laterally with each other. This eventually forms a planar, fenestrated sheet. Finally, the edges of the cell plate are fused with the parental cell wall to complete the cytokinesis. The plant cell division is described in figure 1.

Figure 1: Plant Cell Cycle

During meiosis, plant gametes are not produced directly. The alteration of the generations is observed in some algae and land plants. The haploid spores are produced by the diploid sporophyte generation. Again, these spores are multiplied by mitosis which ultimately leads to haploid gametophyte generation. This generation gives rise to the gametes without undergo the meiosis.

In plants

The fact that most plant cells undergo extensive size increase unaccompanied by cell division is an important distinction between growth in plants and in animals. Daughter cells arising from cell division behind the tip of the plant root or shoot may undergo great increases in volume. This is accomplished through uptake of water by the cells the water is stored in a central cavity called a vacuole. The intake of water produces a pressure that, in combination with other factors, pushes on the cellulose walls of the plant cells, thereby increasing the length, girth, and stiffness ( turgor) of the cells and plant. In plants, much of the size increase occurs after cell division and results primarily from an increase in water content of the cells without much increase in dry weight.

The very young developing plant embryo has many cells distributed throughout its mass that undergo the cycle of growth and cell division. As soon as the positions of the root tip, shoot tip, and embryonic leaves become established, however, the potential for cell division becomes restricted to cells in certain regions called meristems. One meristematic centre lies just below the surface of the growing root all increases in the number of cells of the primary root occur at this point. Some of the daughter cells remain at the elongating tip and continue to divide. Other daughter cells, which are left behind in the root, undergo the increase in length that enables the new root to push deeper into the soil. The same general plan is evident in the growing shoot of higher plants, in which a restricted meristematic region at the tip is responsible for the formation of the cells of the leaves and stem cell elongation occurs behind this meristematic centre. The young seedling secondarily develops cells associated with the vascular strands of phloem and xylem—tissues that carry water to the leaves from the soil and sugar from the leaves to the rest of the plant. These cells can divide again, providing new cell material for development of a woody covering and for more elaborate vascular strands. Hence, the growth of higher plants—i.e., those aspects involving both the pattern of stems, leaves, and roots and the increase in bulk—results primarily from cell division at the meristem followed by a secondary increase in size because of water uptake. These activities occur throughout the period of plant growth.

The first stage in cell division is the duplication of all a cell's DNA. In meiosis, the cell division that results in egg or sperm cells, the initial cell starts with 23 pairs of chromosomes -- that is, 46 separate strands of DNA. After duplication, the cell has 46 pairs of chromosomes, and sends 23 pairs of chromosomes to each side. Then the cell divides. In meiosis in the female the final step, the cytokinesis, is shifted way over to one side. So each of the resulting daughters has a full set of 23 pairs of chromosomes, but one has hardly any cytoplasm, while the other has almost all. The one with hardly any cytoplasm is called a polar body.

The next cell division of meiosis happens like the first, except for one key step: the DNA does not duplicate. Instead, the 23 pairs of chromosomes separate from each other. Each side of the cell then has 23 single chromosomes -- that's half the number in a normal cell, so the two daughters are called haploid. Once the chromosomes have separated, the cell divides again. And once again, in the female, cytokinesis is very asymmetric. One part gets almost all the cytoplasm while the other gets almost none. Again, the small portion is called a polar body. The initial cell divided into one polar body and a larger daughter cell. Each of those two divide again. The polar body divides into two daughter polar bodies, and the larger daughter cell divides into another polar body and an egg cell.

Physics is the new biology

They’ve done their chemistry and genetics. Now scientists are ready to explore the mechanics of being alive.

Amy E. Shyer is watching a movie on her laptop.

It’s a stop-motion clip her lab has created of cells on the move. And it reveals a fundamental truth about why cells do what they do.

Shyer’s film shows what happens when skin cells, extracted from chicken embryos, are spread across a membrane that has just the right degree of rigidity. Frame by frame, the cells jostle and nudge one another until they begin to form small clumps. In living birds, these clumps would eventually become follicles, which would in turn sprout feathers.

Conventional wisdom says that the subtle dance these skin cells perform must be choreographed by genes buried deep within their nuclei. Those genes, so the story goes, express protein molecules that signal the cells to arrange themselves in patterns, migrating to form bits of tissue.

This model of morphogenesis, the process by which an organ takes shape, has been reinforced by decades of research that puts DNA at the center of all biological processes, from the healthy evolution of cells and tissues to the development of diseases like cancer and Alzheimer’s. As a result, says A. James Hudspeth, head of the Laboratory of Sensory Neuroscience, “biology has been a monoculture for the last two or three decades,” with scientists focused on using the tools of molecular biology to harvest the answers buried in our DNA.

That approach yields a theory of life that is simple and organized—DNA tells our cells what to do, and they do it—but that doesn’t tell the full story. A growing number of researchers are finding that cells are capable of responding to more than just their own DNA, and that genomics and biochemistry can’t explain everything.

Shyer and Hudspeth are interested in biomechanics: the same principles of force and motion, first established by Galileo and Newton, that allow engineers to build bridges and launch satellites. What they are finding is that the forces that act on cells, exerted by their neighbors and by the surfaces they live on—even the movements those cells make as they squirm, crawl, and otherwise go about their business—can be as essential to their functioning as genes and proteins, and may sometimes in fact trigger changes in gene expression and biochemistry.

The results can be surprising, even counterintuitive. Shyer’s research, for instance, indicates that the skin cells busily aggregating under her microscope are moving around not because of cues they receive from biochemical messaging, but only from the forces they exert as they push and pull themselves into formation.

“The cells are self-organizing,” explains Shyer, “and they’re doing it based on physical interactions.”

8,325The average number of feathers on a Plymouth Rock chicken.

More broadly, her findings suggest that purely mechanical processes—ones that emerge from the physical interactions of moving cells as they exert force and respond to it—are just as central to morphogenesis as genes and the biochemical signals they regulate. They may even, in some cases, trigger the genetic and biochemical processes that have occupied center stage for so long.

This mechanically oriented perspective is gaining currency across the biological sciences. Researchers are now exploring the biomechanics of phenomena ranging from hearing to DNA replication, often using technologies of their own invention. In so doing, they hope to illuminate the fundamental mechanisms that drive both normal and abnormal development, understand how diseases originate, and even create new opportunities for treatment and prevention.

Shyer, who is head of the Laboratory of Morphogenesis, first became interested in biomechanics as a graduate student at Harvard, where she worked to understand how the intestine develops its signature array of loops and coils.

According to the central dogma of her field, that configuration ought to have originated in a special pattern of gene expression—a chain reaction in which the activation of one gene after another produces a series of molecular events that mold the developing tissue. But try as they might, Shyer and her colleagues could not find such a pattern.

Instead, they discovered that the intestine’s distinctive shape emerged from what applied mathematicians and civil engineers call a “buckling problem”: the same phenomenon that causes the columns in a building to bend and warp under stress.

Mechanical events can sometimes drive molecular ones, and not the other way around.

For Shyer, the realization that an entirely mechanical process could determine the form of a biological organ was an epiphany. She set about trying to find other examples and chose, as her model, avian skin. Chick embryos are easy to work with—they are a staple in developmental biology—and the follicles they develop closely resemble the ones from which human hair grows.

Previously, scientists hypothesized that the clumping behavior shown in Shyer’s stop-motion movie was driven by a unique gene expression pattern that caused cells to congregate around polka-dot concentrations of proteins. One particular protein, beta-catenin—which, among other things, helps cells adhere to one another— was thought to coordinate the entire process.

Recently, however, Shyer and co-author Alan Rodrigues, showed that avian skin cells need no such master regulator to begin rearranging themselves. When she removed beta-catenin from the picture, the cells still happily formed little clumps, so long as the membrane they rested on was, like the bed in the story of Goldilocks and the Three Bears, neither too hard nor too soft.

Further experiments revealed that, once this clustering of cells was under way, it caused beta-catenin to accumulate in the cells’ nuclei, presumably triggering the gene-expression changes required for follicle formation to proceed. These findings added considerably to our understanding of skin development, advancing a narrative in which beta-catenin, though still important, was no longer the all-powerful biochemical puppet master. Shyer and Rodrigues also illustrated how mechanical events can sometimes drive molecular ones, and not the other way around.

Shyer and Rodrigues, a senior staff scientist in the lab, suspect that in nature, embryonic follicle development probably involves a continuous give-and-take between mechanical and molecular processes, with changes on one side triggering responses on the other. Elucidating the precise sequence of mechanical and molecular steps in that feedback loop should help researchers understand human skin morphogenesis and enable them to grow more realistic skin tissue in the lab for research purposes.

In addition, the Shyer lab’s work may spur the development of powerful tools for studying and treating disease. Their discoveries, for example, could lead to improvements in organoids, small lab-grown simulacra of human organs such as brains and livers that hold great potential for biomedical research and regenerative medicine. These ersatz mini-organs might one day allow researchers to more effectively study the development of diseases and to test new drugs more realistically than can be done with rats and mice.

There could be other payoffs as well. Rodrigues and Shyer are currently investigating the mechanical underpinnings of tumor formation in hopes of developing novel strategies for treating cancer—strategies that look beyond the bewildering assortment of genetic errors that can cause cells to turn cancerous and instead address the mechanical processes by which tumors grow and evolve.

“Cancer is fundamentally a physical problem, and it’s related to how cells and tissues behave,” Shyer explains. As a result, drugs that target the molecular mistakes that generate cancer cells could be even more effective if they were combined with treatments that addressed the physical events involved in tumor development.

“Mechanics can’t just be a side dish to the way we think about biology and development,” she says. “Its power lies in how we can connect it to what we know about how genes are expressed and regulated.”

Shyer’s findings raise an important question: If mechanical forces can induce cells to change behavior, how do cells detect these forces in the first place? In other words, how does a cell “feel” when it’s being nudged by a neighbor, or whether the surface it’s resting on is squishy or stiff?

Gregory M. Alushin, head of the Laboratory of Structural Biophysics and Mechanobiology, is attempting to solve these mysteries with a combination of approaches, including a cutting-edge form of electron microscopy.

Wound healing after laser in situ keratomileusis and photorefractive keratectomy

Fabricio Witzel de Medeiros , Steven E Wilson , in Ocular Disease , 2010

Mitosis and migration of stromal cells

Mitosis and migration of stromal cells are noted approximately 8–12 hours after the initial corneal injury. 13 Initially, most cells undergoing mitosis appear to be keratocytes, but corneal fibroblasts and other cells may make subsequent contributions to this response. This cellular mitosis response provides corneal fibroblasts and other cells that participate in corneal wound healing and replenish the stroma. Once again, localization of the stromal mitosis response is related to the type of injury. Thus, in PRK stromal mitosis tends to occur in the anterior stroma, as well as in the peripheral and posterior stroma outside the zone of apoptosis ( Figure 3.2 ). In LASIK, stromal mitosis occurs at the periphery of the flap where the epithelium was injured, and anterior and posterior to the lamellar cut.

Mitosis and migration of stromal cells are regulated by cytokines released from the epithelium and its basement membrane. For example, PDGF is produced by corneal epithelium and bound to basement membrane due to heparin-binding properties of the cytokine. It is released from the epithelial basement membrane after injury and stimulates mitosis of corneal fibroblasts. It is also highly chemotactic to corneal fibroblasts, tending to attract them to the source of the cytokine. Thus, in PRK, for example, PDGF released from the injured epithelium and basement membrane stimulates surviving keratocytes in the peripheral and posterior stroma to undergo mitosis and the daughter cells are attracted to the ongoing PDGF release and repopulate the anterior stroma. Other cytokines such as TGF-β also likely contribute to this keratocyte/corneal fibroblast mitosis and migration. 2

Corneal fibroblasts derived from keratocytes produce collagen, glycosaminoglycans, collagenases, gelatinases, and metalloproteinases 18 used to restore corneal stromal integrity and function. These cells also produce cytokines such as EGF, HGF, and KGF that direct mitosis, migration, and differentiation of the overlying healing epithelium. 1,2,19 After total epithelialization, the fibronectin clot disappears and the nonkeratinized stratified epithelium is re-established. 11,12,20–22

Cells in Reverse

Even all the plastic surgeons in Hollywood can&rsquot turn back the hands of time. But scientists recently found a way to rewind a seemingly irreversible biological process.


Putting cells in reverse. I'm Bob Hirshon and this is Science Update.

For the first time, scientists have reversed the process of cell division: a trick once thought to be as impossible as un-ringing a bell. Molecular biologist Gary Gorbsky of the Oklahoma Medical Research Foundation led the effort. By tinkering with proteins that regulate the process, they turned the clock back from the end of the cell cycle to the middle.

And specifically, the end stages, where they&rsquore actually divided in half, we&rsquove been able to reverse that process, and go from the stage at which you have two cells back to the stage at which you have a single cell.

This worked only when the divided cells hadn&rsquot completely finished separating. The implications aren&rsquot clear yet, but the technique could be useful to cancer researchers, who are always looking for ways to keep rogue cells under control. I'm Bob Hirshon, for AAAS, the science society.

Making Sense of the Research

The process that Gorbsky&rsquos team reversed is mitosis, which you may have studied in biology class. In mitosis, a cell divides by duplicating its chromosomes (the strands of DNA containing genes), ripping them apart, and splitting the cell in two. Mitosis is divided into several stages (see &ldquoGoing Further&rdquo for more information). Gorbsky&rsquos team took cells that were in the final phase of cell division, called cytokinesis, in which the chromosomes have separated and the cell has split in two, and rewound them to metaphase, in which the duplicate chromosomes are still attached to each other, and lined up in the center of a single cell.

You can see why this is so groundbreaking. It&rsquos one thing to glue a broken vase back together, but could you actually restore it to its original form&mdashwith no cracks, as if it were never dropped? What Gorbsky&rsquos team did here is just as amazing. It&rsquos almost as if they turned back the hands of time, at least for this particular cell.

But Gorbsky&rsquos team couldn&rsquot just make two completely separate cells find each other across a crowded petri dish and smush back into one. Rather, they had to act while the divided cells were still connected by the midbody: a small, plug-like structure that buttons the new cells together for several hours after the original cell splits in two. In other words, the reversal could happen only if the job wasn&rsquot quite finished.

So how did they do it? Basically, by fiddling with an enzyme that plays a key role in controlling mitosis. The enzyme, in turn, is controlled by a protein called an activator. Near the end of the cell division process, this activator protein is destroyed, which turns the enzyme off and signals the cell to finish the job.

But Gorbsky&rsquos team figured out a way to keep this activator protein around, and to turn the enzyme on and off directly, using another chemical. So, basically, they developed a way to &ldquomanually&rdquo stop the cell cycle before it was completely finished. Then they reactivated the enzyme (with the activator protein still present). That&rsquos when something surprising happened. Instead of ditching the little midbody and splitting apart completely, the divided cells actually fused back together and rewound to the middle stage of mitosis. It&rsquos as if they hit some kind of a biological reset button, fooling the cell into retracing its steps.

This study is a kind of basic research: work that scientists do to understand the world, rather than to invent something or solve a specific, practical problem. Prior to this study, scientists suspected that the destruction of the activator protein was partly responsible for making the cell cycle run forwards. By showing that keeping the protein around makes the cell cycle run backwards, Gorbsky&rsquos team not only confirmed this, but also discovered something that no one knew you could do before.

Looking to the future, this knowledge may have many possible applications. As the story suggests cancer therapy is a strong possibility. Cancer, as you may know, is basically the result of rogue cells growing and dividing out of control. If scientists can not only stop these cells from dividing, but also reverse the process, it could open the door to a whole new kind of treatment.

Now try and answer these questions:

  1. What is mitosis?
  2. What exactly did this study accomplish?
  3. How did this research both confirm an existing hypothesis and discover something new?
  4. Can you think of other reasons why scientists would want to reverse the process of cell division?

The Cell Cycle, from Cells Alive! features an animation of the cell cycle, the sequence of activities exhibited by cells. A detailed explanation of each cell phase is included on the page.

The Access Excellence activity Chromosome Shuffle is designed to clarify and reinforce student understanding of the cellular processes of mitosis and meiosis.


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Watch the video: Mitosis Rap: Mr. Ws Cell Division Song (January 2022).