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Cell division[edit]

Cell division is the process by which a parent cell divides into two or more daughter cells.[1] Cell division usually occurs as part of a larger cell cycle. In eukaryotes, there are two distinct types of cell division: a vegetative division, whereby each daughter cell is genetically identical to the parent cell (mitosis), and a reproductive cell division, whereby the number of chromosomes in the daughter cells is reduced by half to produce haploid gametes (meiosis).[2] Meiosis results in four haploid daughter cells by undergoing one round of DNA replication followed by two divisions. Homologous chromosomes are separated in the first division, and sister chromatids are separated in the second division. Both of these cell division cycles are used in the process of sexual reproduction at some point in their life cycle. Both are believed to be present in the last eukaryotic common ancestor.

Prokaryotes (bacteria) undergo a vegetative cell division known as binary fission, where their genetic material is segregated equally into two daughter cells. While binary fission many be the means of division by most prokaryotes, there are alternative manners of division, such as budding, that have been observed. All cell divisions, regardless of organism, are preceded by a single round of DNA replication.

For simple unicellular microorganisms such as the amoeba, one cell division is equivalent to reproduction – an entire new organism is created. On a larger scale, mitotic cell division can create progeny from multicellular organisms, such as plants that grow from cuttings. Mitotic cell division enables sexually reproducing organisms to develop from the one-celled zygote, which itself was produced by meiotic cell division from gametes.[3][4] After growth, cell division by mitosis allows for continual construction and repair of the organism.[5] The human body experiences about 10 quadrillion cell divisions in a lifetime.[6]

The primary concern of cell division is the maintenance of the original cell's genome. Before division can occur, the genomic information that is stored in chromosomes must be replicated, and the duplicated genome must be separated cleanly between cells.[7] A great deal of cellular infrastructure is involved in keeping genomic information consistent between generations.

Phases of eukaryotic cell division[edit]

Interphase[edit]

Interphase is the process a cell must go through before mitosis, meiosis, and cytokinesis.[8] Interphase consists of three main phases: G1, S, and G2. G1 is a time of growth for the cell where specialized cellular functions occur in order to prepare the cell for DNA Replication.[9] There are checkpoints during interphase that allow the cell to be either advance or halt further development. In S phase, the chromosomes are replicated in order for the genetic content to be maintained.[10] During G2, the cell undergoes the final stages of growth before it enters the M phase, where spindles are synthesized. The M phase, can be either mitosis or meiosis depending on the type of cell. Germ cells, or gametes, undergo meiosis, while somatic cells will undergo mitosis. After the cell proceeds successfully through the M phase, it may then undergo cell division through cytokinesis. The control of each checkpoint is controlled by cyclin and cyclin-dependent kinases. The progression of interphase is the result of the increased amount of cyclin. As the amount of cyclin increases, more and more cyclin dependent kinases attach to cyclin signaling the cell further into interphase. At the peak of the cyclin attached to the cyclin dependent kinases this system pushes the cell out of interphase and into the M phase, where mitosis, meiosis, and cytokinesis occur.[11] There are three transition checkpoints the cell goes through before entering the M phase. The most important being the G1-S transition checkpoint. If the cell does not pass this checkpoint, then the cell will exit the cell cycle.[12]

Prophase[edit]

Prophase is the first stage of division. The nuclear envelope is broken down, long strands of chromatin condense to form shorter more visible strands called chromosomes, the nucleolus disappears, and microtubules attach to the chromosomes at the kinetochores present in the centromere.[13] Microtubules associated with the alignment and separation of chromosomes are referred to as the spindle and spindle fibers. Chromosomes will also be visible under a microscope and will be connected at the centromere. During this condensation and alignment period in meiosis, the homologous chromosomes undergo a break in their double-stranded DNA at the same locations followed by a recombination of the now fragmented parental DNA strands into non-parental combinations, known as crossing over.[14] This process is evidenced to be caused in a large part by the highly conserved Spo11 protein through a mechanism similar to that seen with toposomerase in DNA replication and transcription.[15]

Metaphase[edit]

In metaphase, the centromeres of the chromosomes convene themselves on the metaphase plate (or equatorial plate), an imaginary line that is equidistant from the two centrosome poles and held together by complex complexes known as cohesins. Chromosomes line up in the middle of the cell by microtubule organizing centers (MTOCs) pushing and pulling on centromeres of both chromatids thereby causing the chromosome to move to the center. At this point the chromosomes are still condensing and are currently one step away from being the most coiled and condensed they will be, and the spindle fibers have already connected to the kinetochores.[16] During this phase all the microtubules, with the exception of the kinetochores, are in a state of instability promoting their progression towards anaphase.[17] At this point, the chromosomes are ready to split into opposite poles of the cell towards the spindle to which they are connected.[18]

Anaphase[edit]

Anaphase is a very short stage of the cell cycle and occurs after the chromosomes align at the mitotic plate. Kinetochores emit anaphase-inhibition signals until their attachment to the mitotic spindle. Once the final chromosome is properly aligned and attached the final signal dissipates and triggers the abrupt shift to anaphase.[17] This abrupt shift is caused by the activation of the anaphase-promoting complex and its function of tagging degradation of proteins important towards the metaphase-anaphase transition. One of these proteins that is broken down is securin which through its breakdown releases the enzyme separase that cleaves the cohesin rings holding together the sister chromatids thereby leading to the chromosomes separating.[19] After the chromosomes line up in the middle of the cell, the spindle fibers will pull them apart. The chromosomes are split apart as the sister chromatids move to opposite sides of the cell.[20] While the sister chromatids are being pulled apart, the cell and plasma are elongated by non-kinetochore microtubules.[21]

Telophase[edit]

Telophase is the last stage of the cell cycle in which a cleavage furrow splits the cells cytoplasm (cytokinesis) and chromatin. This occurs through the synthesis of a new nuclear envelopes that forms around the chromatin gathered at each pole and the reformation of the nucleolus as the chromosomes decondense their chromatin back to the loose state it possessed during interphase.[22][23] The division of the cellular contents is not always equal and can vary by cell type as seen with oocyte formation where one of the four daughter cells possess the majority of the cytoplasm.[4]

Variants[edit]

Cells are broadly classified into two main categories: simple, non-nucleated prokaryotic cells, and complex, nucleated eukaryotic cells. Due to their structural differences, eukaryotic and prokaryotic cells do not divide in the same way. Also, the pattern of cell division that transforms eukaryotic stem cells into gametes (sperm cells in males or egg cells in females), termed meiosis, is different from that of the division of somatic cells in the body. Image of the mitotic spindle in a human cell showing microtubules in green, chromosomes (DNA) in blue, and kinetochores in red.

Degradation[edit]

Multicellular organisms replace worn-out cells through cell division. In some animals, however, cell division eventually halts. In humans this occurs, on average, after 52 divisions, known as the Hayflick limit. The cell is then referred to as senescent. With each division the cells telomeres, protective sequences of DNA on the end of a chromosome that prevent degradation of the chromosomal DNA, shorten. This shortening has been correlated to negative effects such as age related diseases and shortened lifespans in humans.[24][25] Cancer cells, on the other hand, are not thought to degrade in this way, if at all. An enzyme complex called telomerase, present in large quantities in cancerous cells, rebuilds the telomeres through synthesis of telomeric DNA repeats, allowing division to continue indefinitely.[26]

History[edit]

A cell division under microscope was first discovered by German botanist Hugo von Mohl in 1835 as he worked over Green algae Cladophora glomerata.[27]

In 1943, cell division was filmed for the first time[28] by Kurt Michel using a phase-contrast microscope.[29]


References[edit]

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  3. ^ Gilbert, Scott F. (2000). "Spermatogenesis". Developmental Biology. 6th edition.
  4. ^ a b Gilbert, Scott F. (2000). "Oogenesis". Developmental Biology. 6th edition.
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  12. ^ Hartwell, Leland H.; Toczyski, David P.; Paulovich, Amanda G. (1997-02-07). "When Checkpoints Fail". Cell. 88 (3): 315–321. doi:10.1016/S0092-8674(00)81870-X. ISSN 0092-8674. PMID 9039258.
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  14. ^ Lewontin, Richard C.; Miller, Jeffrey H.; Gelbart, William M.; Griffiths, Anthony JF (1999). "The Mechanism of Crossing-Over". Modern Genetic Analysis.
  15. ^ Keeney, Scott (2001), "Mechanism and control of meiotic recombination initiation", Current Topics in Developmental Biology, Elsevier, pp. 1–53, ISBN 9780121531522, retrieved 2019-04-15
  16. ^ "Researchers Shed Light On Shrinking Of Chromosomes". ScienceDaily. Retrieved 2019-04-14.
  17. ^ a b Walter, Peter; Roberts, Keith; Raff, Martin; Lewis, Julian; Johnson, Alexander; Alberts, Bruce (2002). "Mitosis". Molecular Biology of the Cell. 4th edition.
  18. ^ Elrod, Susan L. (2010). Schaum's outlines : genetics. Elrod, Susan L. (5th ed ed.). New York: Mcgraw-Hill. p. 8. ISBN 9780071625036. OCLC 473440643. {{cite book}}: |edition= has extra text (help)
  19. ^ Brooker, Amanda S.; Berkowitz, Karen M. (2014), "The Roles of Cohesins in Mitosis, Meiosis, and Human Health and Disease", Methods in Molecular Biology, Springer New York, pp. 229–266, ISBN 9781493908875, retrieved 2019-04-15
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  21. ^ "Campbell Biology in Focus . By Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Robert B. Jackson, and Jane B. Reece. Boston (Massachusetts): Pearson. $146.67. xxxix + 905 p.; ill. + A-1 - A-34; B-1; C-1; D-1; E-1 - E-2; F-1 - F-3; CR-1 - CR-6; G-1 - G-34; I-1 - I-48 (index). ISBN: 978-0-321-81380-0. 2014". The Quarterly Review of Biology. 88 (3): 242–242. 2013-9. doi:10.1086/671541. ISSN 0033-5770. {{cite journal}}: Check date values in: |date= (help)
  22. ^ Dekker, Job (2014-11-25). "Two ways to fold the genome during the cell cycle: insights obtained with chromosome conformation capture". Epigenetics & Chromatin. 7 (1). doi:10.1186/1756-8935-7-25. ISSN 1756-8935.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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  24. ^ Jiang, Hong; Schiffer, Eric; Song, Zhangfa; Wang, Jianwei; Zürbig, Petra; Thedieck, Kathrin; Moes, Suzette; Bantel, Heike; Saal, Nadja (2008-08-12). "Proteins induced by telomere dysfunction and DNA damage represent biomarkers of human aging and disease". Proceedings of the National Academy of Sciences of the United States of America. 105 (32): 11299–11304. doi:10.1073/pnas.0801457105. ISSN 1091-6490. PMC PMCPMC2516278. PMID 18695223. {{cite journal}}: Check |pmc= value (help)
  25. ^ Cawthon, Richard M.; Smith, Ken R.; O'Brien, Elizabeth; Sivatchenko, Anna; Kerber, Richard A. (2003-02-01). "Association between telomere length in blood and mortality in people aged 60 years or older". Lancet (London, England). 361 (9355): 393–395. doi:10.1016/S0140-6736(03)12384-7. ISSN 0140-6736. PMID 12573379.
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