Did crossing over occur in mitosis meiosis or both

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Cells divide and reproduce in two ways, mitosis and meiosis. Mitosis results in two identical daughter cells, whereas meiosis results in four sex cells. Below we highlight the keys differences and similarities between the two types of cell division.

It can actually on very rare occasions however, it is also highly problematic and generally creates deleterious mutations and can inactivate genes. Depending on the location of the cell and the cross-over within the genome, it can also contribute to the formation of cancer. For instance, in the case of retinoblastoma, if there is one mutated copy of RAS on one chromosome and a normal copy on the other and mitotic crossing over occurs, then you can potentially remove the protective nonmutant copy of RAS from one of the daughter cells. This cell is then one step closer to becoming tumorgenic.

Thus, one reason this may not occur ordinarily is to reduce the chance of causing such a cancer. As for why it does occur on the rare times it does, I am not certain as of the time of writing this.

Reference: The Biology of Cancer, by Robert A. Weinberg

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Figure 2: Examples of polytene chromosomes

Pairing of homologous chromatids results in hundreds to thousands of individual chromatid copies aligned tightly in parallel to produce giant, "polytene" chromosomes.

Although he did not know it, Walther Flemming actually observed spermatozoa undergoing meiosis in 1882, but he mistook this process for mitosis. Nonetheless, Flemming did notice that, unlike during regular cell division, chromosomes occurred in pairs during spermatozoan development. This observation, followed in 1902 by Sutton's meticulous measurement of chromosomes in grasshopper sperm cell development, provided definitive clues that cell division in gametes was not just regular mitosis. Sutton demonstrated that the number of chromosomes was reduced in spermatozoan cell division, a process referred to as reductive division. As a result of this process, each gamete that Sutton observed had one-half the genetic information of the original cell. A few years later, researchers J. B. Farmer and J. E. S. Moore reported that this process—otherwise known as meiosis—is the fundamental means by which animals and plants produce gametes (Farmer & Moore, 1905).

The greatest impact of Sutton's work has far more to do with providing evidence for Mendel's principle of independent assortment than anything else. Specifically, Sutton saw that the position of each chromosome at the midline during metaphase was random, and that there was never a consistent maternal or paternal side of the cell division. Therefore, each chromosome was independent of the other. Thus, when the parent cell separated into gametes, the set of chromosomes in each daughter cell could contain a mixture of the parental traits, but not necessarily the same mixture as in other daughter cells.

To illustrate this concept, consider the variety derived from just three hypothetical chromosome pairs, as shown in the following example (Hirsch, 1963). Each pair consists of two homologues: one maternal and one paternal. Here, capital letters represent the maternal chromosome, and lowercase letters represent the paternal chromosome:

• Pair 1: A and a
• Pair 2: B and b
• Pair 3: C and c

When these chromosome pairs are reshuffled through independent assortment, they can produce eight possible combinations in the resulting gametes:

• A B C
• A B c
• A b c
• A b C
• a B C
• a B c
• a b C
• a b c

A mathematical calculation based on the number of chromosomes in an organism will also provide the number of possible combinations of chromosomes for each gamete. In particular, Sutton pointed out that the independence of each chromosome during meiosis means that there are 2n possible combinations of chromosomes in gametes, with "n" being the number of chromosomes per gamete. Thus, in the previous example of three chromosome pairs, the calculation is 23, which equals 8. Furthermore, when you consider all the possible pairings of male and female gametes, the variation in zygotes is (2n)2, which results in some fairly large numbers.

But what about chromosome reassortment in humans? Humans have 23 pairs of chromosomes. That means that one person could produce 223 different gametes. In addition, when you calculate the possible combinations that emerge from the pairing of an egg and a sperm, the result is (223)2 possible combinations. However, some of these combinations produce the same genotype (for example, several gametes can produce a heterozygous individual). As a result, the chances that two siblings will have the same combination of chromosomes (assuming no recombination) is about (3/8)23, or one in 6.27 billion. Of course, there are more than 23 segregating units (Hirsch, 2004).

While calculations of the random assortment of chromosomes and the mixture of different gametes are impressive, random assortment is not the only source of variation that comes from meiosis. In fact, these calculations are ideal numbers based on chromosomes that actually stay intact throughout the meiotic process. In reality, crossing-over between chromatids during prophase I of meiosis mixes up pieces of chromosomes between homologue pairs, a phenomenon called recombination. Because recombination occurs every time gametes are formed, we can expect that it will always add to the possible genotypes predicted from the 2n calculation. In addition, the variety of gametes becomes even more unpredictable and complex when we consider the contribution of gene linkage. Some genes will always cosegregate into gametes if they are tightly linked, and they will therefore show a very low recombination rate. While linkage is a force that tends to reduce independent assortment of certain traits, recombination increases this assortment. In fact, recombination leads to an overall increase in the number of units that assort independently, and this increases variation.

While in mitosis, genes are generally transferred faithfully from one cellular generation to the next; in meiosis and subsequent sexual reproduction, genes get mixed up. Sexual reproduction actually expands the variety created by meiosis, because it combines the different varieties of parental genotypes. Thus, because of independent assortment, recombination, and sexual reproduction, there are trillions of possible genotypes in the human species.

Cell division occurs as a part of the “cell cycle”. Just like your day has a routine from day to night, cells have routines of their own. The cell cycle is generally described as consisting of four main phases: G1, S phase, G2 and mitosis (or meiosis). Cells can also take a break from the grind of the cell cycle, in a state called G0 or senescence (note that some cells are permanently in G0). External growth factors can stimulate cells in G1 or G0 to proceed through the rest of the cycle, an example is Nerve Growth Factor (NGF), which promotes neuron growth. The restriction point is a special “point of no return” in G1 when cells no longer respond to removal of growth factors and will continue to progress to S phase no matter what. There are also internal signals that tell the cell to progress, these proteins are called cyclins and the cyclin that promotes mitosis is called cyclin B. S phase is especially important as this is the point at which the cell’s entire genome is duplicated through the process of semi-conservative DNA replication.

The stages of mitosis are interphase, prophase, metaphase, anaphase and telophase, sometimes followed by cytokinesis. “Interphase” is a blanket term which describes all the stages before mitosis, that is: G1, S and G2 phases. The stages of meiosis are interphase, prophase I, metaphase I, anaphase I, telophase I, cytokinesis I, prophase II, metaphase II, anaphase II, telophase II, and finally cytokinesis II. See our detailed explanation below:

Another way to understand the progression of mitosis and meiosis is by thinking about what is happeningto the chromosomes, centrosomes, nuclear membrane and cell plasma membrane at each stage of the process. Here we show how to do this for mitosis, why not try to recreate this table for meiosis?

Mnemonics are also helpful, for example a useful mnemonic to remember the order of the steps in mitosis is “I Prefer Mating At Teatime” – Chamillionaire.

The process of cell division is an intricate dance of molecular machinery that has fascinated researchers for hundreds of years. Advances in microscopy have had a huge impact on the field, from its humble beginnings observing metaphase chromosomes under the light microscope, to more sophisticated technologies today that can ask questions at the molecular level. Research into the cell cycle has also been highly rewarded, with the 2001 Nobel Prize in Physiology/Medicine being awarded to Tim Hunt, Paul Nurse and Leland Hartwell for their joint discovery of cyclins and cyclin-dependent kinases: the key regulators of the cell cycle [6]. However, despite our progress, many questions still remain.

While there is only one way for mitosis to go right, there are many ways for it to go wrong. For example, in early mitosis, if there are incorrect contacts between microtubules and chromosomes, chromosomes can become misaligned, which can lead to incorrect segregation of sister chromatids. In late mitosis, how is the cell certain that the time is right to perform cytokinesis? The chromosome passenger complex (CPC) is a molecular guardian angel that acts at many stages of mitosis to safeguard the fidelity of the process. At the start of mitosis, the CPC localises all over the chromosomes and acts to modify chromatin, during mitosis it moves to the chromosome centromeres to prevent incorrect microtubule attachments and before cytokinesis the CPC finds its way to the central spindle. Therefore, a question of ongoing research is how does the CPC elegantly re-localise throughout mitosis to save the day?

•Vader, G., Medema, R. H., & Lens, S. M. (2006). The chromosomal passenger complex: guiding Aurora-B through mitosis. The Journal of cell biology, 173(6), 833-837.

•Kabeche, L., Nguyen, H. D., Buisson, R., & Zou, L. (2018). A mitosis-specific and R loop–driven ATR pathway promotes faithful chromosome segregation. Science, 359(6371), 108-114.

You might remember from above that it is the protein cohesin that holds together sister chromatids in metaphase of mitosis and metaphase II of meiosis. However, in meiosis I homologous chromosomes must be held together in metaphase I, before these ties are swiftly broken during anaphase I. This feat is performed by a miraculous cellular zipper called the synaptonemal complex (SC). This zipper must be strong enough to hold chromosomes together, but it must also be disassembled equally efficiently, otherwise homologous chromosomes will not accurately segregate in anaphase I, leading to a potentially disastrous genetic inequality in the daughter cells. How exactly this zipper disassembles is a hot topic of research.

•Argunhan, B., Tsubouchi, T., & Tsubouchi, H. (2018). Polo is not solo in meiosis. Cell Cycle, 17(3), 273-274.

•Gao, J., & Colaiácovo, M. P. (2017). Zipping and unzipping: protein modifications regulating synaptonemal complex dynamics. Trends in Genetics.

References

1)Bennett, M. D. (1977). The time and duration of meiosis. Phil. Trans. R. Soc. Lond. B, 277(955), 201-226.

2)Jett, J. H. (2015). How long does it take a cell to divide? Cytometry Part A, 87(5), 383-384.

3)Brewer, B. J., Chlebowicz-Sledziewska, E., & Fangman, W. L. (1984). Cell cycle phases in the unequal mother/daughter cell cycles of Saccharomyces cerevisiae. Molecular and cellular biology, 4(11), 2529-2531.

4)Clift, D., & Schuh, M. (2013). Restarting life: fertilization and the transition from meiosis to mitosis. Nature reviews Molecular cell biology, 14(9), 549.

5)Paweletz, N. (2001). Walther Flemming: pioneer of mitosis research. Nature Reviews Molecular Cell Biology, 2(1), 72.

6)Nurse, P. M. (2002). Nobel Lecture: Cyclin dependent kinases and cell cycle control. Bioscience reports, 22(5), 487-499.