36.4:
Meiosis vs. Mitosis
Mitosis and meiosis primarily differ from each other with respect to the number of steps involved, genetic recombination events, and final chromosome and daughter cell numbers.
Most eukaryotic cells divide by mitosis, an equational division, where each diploid parent cell produces two identical diploid daughter cells.
However, each diploid germ cell divides into four genetically distinct haploid daughter cells through meiosis, a reductional division.
Mitosis is a four-stage process – prophase, metaphase, anaphase, and telophase. Meiosis goes through these four stages twice without an intermediate DNA synthesis phase.
The prophase stage of mitosis is shorter and does not involve the pairing of homologous chromosomes or any recombination. Therefore, all the daughter cells are genetically identical.
In meiosis, prophase I is the longest phase consisting of five substages. In prophase I, two homologous chromosomes pair to form a synaptonemal complex and subsequently recombine to produce four genetically diverse chromatids.
During mitotic metaphase, the individual chromosomes assemble along the equator, whereas during metaphase I of meiosis, pairs of homologous chromosomes align on the equator.
The sister chromatids of each chromosome are held together by cohesin complexes.
The cohesin complexes are completely removed by the end of the mitotic metaphase allowing the sister chromatids to separate and move towards opposite poles.
However, in meiosis I, only the cohesin complexes present on the chromosome arms get detached from the chromatid at the start of the anaphase I, whereas those surrounding the kinetochore remain intact.
Thus, even as the homologous chromosomes are separated and pulled to opposite poles, the sister chromatids remain attached and migrate together.
The second cell division in meiosis II is similar to mitosis. Mitotic anaphase and anaphase II of meiosis involve the separation of two sister chromatids of each homologous chromosome, and subsequent division into two daughter cells – identical and diploid for mitosis but non-identical and haploid for meiosis II.
The daughter cells arising from meiosis are more likely to have chromosome segregation errors than the ones arising from mitosis. Such chromosome segregation errors produce aneuploid cells with an incorrect number of chromosomes which can lead to diseases like Down syndrome.
36.4:
Meiosis vs. Mitosis
Cell division is necessary for growth and reproduction in organisms. Mitosis aids cell growth and development by dividing somatic cells. In contrast, meiosis causes the division of germ cells and plays an essential role in sexual reproduction. Due to their unique functional requirements, mitosis and meiosis differ from each other in multiple aspects.
Before the start of mitosis and meiosis I, the cell synthesizes DNA, resulting in two homologous copies of each chromosome. DNA synthesis is prevented during mitosis and meiosis I by high cyclin-dependent kinase (CDK) activity. This activity stops the formation of pre-replicative complexes and thus does not allow DNA replication to begin. No DNA synthesis occurs before the initiation of meiosis II as CDK activity remains high in both meiosis I and II.
Meiosis and mitosis also employ different damage repair pathways. Accidental DNA damage can result in double-strand breaks (DSBs) in DNA, which can be repaired by either non-homologous DNA end-joining or homologous recombination. In mitosis, accidental and random DSBs are repaired by the homologous recombination repair process. In contrast, pairing and recombination of the homologous chromosomes are a part of meiosis I, and therefore DSBs formation and repair occur in each meiosis cycle. Unlike mitosis, these DSBs are formed at selected places on the chromosome by the endonuclease Spo11.
Errors can occur during chromosome segregation resulting in the production of aneuploid cells. Female meiosis is more error-prone than mitosis and male meiosis. Though the exact reasons for a high error rate in female meiosis still need to be determined, several factors are considered responsible. The single meiosis cycle in an oocyte can take up to 40 years to complete, ending only after fertilization. Such a long duration can cause cohesin deterioration resulting in the premature release of sister chromatids. The chiasmata holding two homologous chromosomes can also slip away with time, affecting the correct orientation and attachment of the bivalents to the meiotic spindle. Also, aging can cause a decrease in the concentration of proteins (e.g., Mad2) involved in the spindle-assembly checkpoint mechanism, which can be another reason for the relatively high error rate in female meiosis.
The missegregation of chromosomes can cause the development of zygotes into abnormal embryos, which often die during fetal development or just after birth. It can also cause genetic diseases like Down syndrome and Turner syndrome. The chances of chromosomal segregation errors have been found to increase with the age of the mother. For example, a woman below 30 years of age has less than a 0.1% chance of having a baby with Down syndrome, whereas the chance increases to 3.5% for a woman who is 45 years old.
Suggested Reading
- Ohkura, Hiroyuki. "Meiosis: an overview of key differences from mitosis." Cold Spring Harbor Perspectives in Biology 7, no. 5 (2015): a015859. https://cshperspectives.cshlp.org/content/7/5/a015859.full.pdf+html
- Duro, Eris, and Adèle L. Marston. "From equator to pole: splitting chromosomes in mitosis and meiosis." Genes & Development 29, no. 2 (2015): 109-122. http://genesdev.cshlp.org/content/29/2/109.full.pdf
- Hauf, Silke, and Yoshinori Watanabe. "Kinetochore orientation in mitosis and meiosis." Cell 119, no. 3 (2004): 317-327. https://www.cell.com/cell/pdf/S0092-8674(04)00996-1.pdf
- Yun, Yan, Janet E. Holt, Simon Lane, Eileen McLaughlin, Julie Merriman, and Keith Jones. "Reduced ability to recover from spindle disruption and loss of kinetochore spindle assembly checkpoint proteins in oocytes from aged mice." Cell cycle 13, no. 12 (2014): 1938-1947. https://www.tandfonline.com/doi/pdf/10.4161/cc.28897