View source for Biology:Cytokinesis

{{Short description|Part of the cell division process}}
[[File:Cytokinesis illustration.svg|thumb|Cytokinesis illustration]]
[[File:Unk.cilliate.jpg|thumb|right|250px|Ciliate undergoing cytokinesis, with the cleavage furrow being clearly visible.]]

'''Cytokinesis''' ({{IPAc-en|ˌ|s|aɪ|t|oʊ|k|ɪ|ˈ|n|iː|s|ɪ|s}}) is the part of the [[Biology:Cell division|cell division]] [[Biology:Biological process|process]] and part of mitosis during which the [[Biology:Cytoplasm|cytoplasm]] of a single eukaryotic cell divides into two daughter cells. Cytoplasmic division begins during or after the late stages of [[Biology:Mitosis|nuclear division]] in [[Biology:Mitosis|mitosis]] and [[Biology:Meiosis|meiosis]]. During cytokinesis the [[Biology:Spindle apparatus|spindle apparatus]] partitions and transports duplicated [[Biology:Chromatid|chromatid]]s into the cytoplasm of the separating daughter [[Biology:Cell|cells]]. It thereby ensures that [[Biology:Chromosome|chromosome]] number and complement are maintained from one generation to the next and that, except in special cases, the daughter cells will be functional copies of the parent cell. After the completion of the [[Biology:Telophase|telophase]] and cytokinesis, each daughter cell enters the [[Biology:Interphase|interphase]] of the [[Biology:Cell cycle|cell cycle]].

Particular functions demand various deviations from the process of symmetrical cytokinesis; for example in [[Biology:Oogenesis|oogenesis]] in animals the ovum takes almost all the cytoplasm and organelles. This leaves very little for the resulting polar bodies, which in most species die without function, though they do take on various special functions in other species.<ref>{{cite journal | author = Schmerler Samuel, Wessel Gary | date = January 2011 | title = Polar Bodies - more a lack of understanding than a lack of respect | journal = Mol Reprod Dev | volume = 78 | issue = 1| pages = 3–8 | doi = 10.1002/mrd.21266 | pmid = 21268179 | pmc = 3164815 }}</ref>
Another form of mitosis occurs in tissues such as [[Biology:Liver|liver]] and [[Biology:Skeletal muscle|skeletal muscle]]; it omits cytokinesis, thereby yielding [[Biology:Multinucleate|multinucleate]] cells.

Plant cytokinesis differs from animal cytokinesis, partly because of the rigidity of plant cell walls. Instead of plant cells forming a cleavage furrow such as develops between animal daughter cells, a dividing structure known as the [[Biology:Cell plate|cell plate]] forms in the cytoplasm and grows into a new, doubled [[Biology:Cell wall|cell wall]] between plant daughter cells. It divides the cell into two daughter cells.

Cytokinesis largely resembles the [[Biology:Prokaryote|prokaryotic]] process of [[Binary fission|binary fission]], but because of differences between prokaryotic and eukaryotic cell structures and functions, the mechanisms differ. For instance, a bacterial cell has a [[Biology:Circular chromosome|Circular chromosome]] (a single chromosome in the form of a closed loop), in contrast to the [[Biology:Linear chromosome|linear]], usually multiple, chromosomes of eukaryote. Accordingly, bacteria construct no mitotic spindle in cell division. Also, duplication of prokaryotic DNA takes place during the actual separation of chromosomes; in mitosis, duplication takes place during the [[Biology:Interphase|interphase]] before mitosis begins, though the daughter [[Biology:Chromatid|chromatid]]s don't separate completely before the [[Biology:Anaphase|anaphase]].

==Etymology and pronunciation==
The word "cytokinesis" ({{IPAc-en|ˌ|s|aɪ|t|oʊ|k|aɪ|ˈ|n|iː|s|ᵻ|s|,_|-|t|ə|-|,_|-|k|ə|-}}{{refn|{{Cite dictionary |url=http://www.lexico.com/definition/cytokinesis |archive-url=https://web.archive.org/web/20200322182541/https://www.lexico.com/definition/cytokinesis |archive-date=2020-03-22 |title=cytokinesis |dictionary=Lexico UK English Dictionary |publisher=[[Organization:Oxford University Press|Oxford University Press]]}} }}{{refn|{{MerriamWebsterDictionary|access-date=2016-01-21|cytokinesis}}}}) uses [[Social:Classical compound|combining forms]] of ''cyto-'' + ''kine-'' + ''-sis'', Neo-Latin from Classical Latin and [[Social:Ancient Greek|Ancient Greek]], reflecting "[[Biology:Cell|cell]]" and ''[[Philosophy:Kinesis|kinesis]]'' ("motion, movement"). It was coined by Charles Otis Whitman in 1887.<ref>Battaglia, Emilio (2009). Caryoneme alternative to chromosome and a new caryological nomenclature. ''Caryologia'' 62 (4): 1–80. [http://www.caryologia.unifi.it/past_volumes/62_4supplement/62-4_supplement.pdf link].</ref>

Origin of this term is from [[Social:Ancient Greek|Greek]] {{lang|grc|κύτος}} (''{{transl|grc|kytos}}'', a hollow), Latin derivative ''{{lang|la|cyto}}'' (cellular), Greek {{lang|el|κίνησις}} (''{{transl|el|kínesis}}'', movement).

== Animal cell ==
[[File:Telophase.svg|300px|thumb|Animal cell telophase and cytokinesis]]

Animal cell cytokinesis begins shortly after the onset of sister [[Biology:Chromatid|chromatid]] separation in the [[Biology:Anaphase|anaphase]] of [[Biology:Mitosis|mitosis]]. The process can be divided to the following distinct steps: anaphase spindle reorganization, division plane specification, actin-myosin ring assembly and contraction, and abscission.<ref name="Fededa-2012">{{cite journal | vauthors = Fededa JP, Gerlich DW | title = Molecular control of animal cell cytokinesis | journal = Nat. Cell Biol. | volume = 14 | issue = 5 | pages = 440–7 | date = May 2012 | pmid = 22552143 | doi = 10.1038/ncb2482| s2cid = 3355851 | hdl = 11336/20338 | hdl-access = free }}</ref> Faithful partitioning of the genome to emerging daughter cells is ensured through the tight temporal coordination of the above individual events by molecular signaling pathways.

===Anaphase spindle reorganization===
Animal cell cytokinesis starts with the stabilization of microtubules and reorganization of the mitotic spindle to form the central spindle. The [[Biology:Central spindle|central spindle]] (or ''spindle midzone'') forms when non-kinetochore microtubule fibers are bundled between the spindle poles. A number of different species including ''H. sapiens'', ''[[Biology:Drosophila melanogaster|D. melanogaster]]'' and ''[[Biology:Caenorhabditis elegans|C. elegans]]'' require the central spindle in order to efficiently undergo cytokinesis, although the specific [[Biology:Phenotype|phenotype]] associated with its absence varies from one species to the next (for example, certain Drosophila cell types are incapable of forming a cleavage furrow without the central spindle, whereas in both ''C. elegans'' embryos and human [[Biology:Tissue culture|tissue culture]] cells a cleavage furrow is observed to form and ingress, but then regress before cytokinesis is complete). 
The process of mitotic spindle reorganization and central spindle formation is caused by the decline of CDK1 activity during anaphase.<ref name="Fededa-2012"/> The decline of CDK1 activity at the metaphase-anaphase transition leads to dephosphorylating of inhibitory sites on multiple central spindle components. First of all, the removal of a CDK1 phosphorylation from a subunit of the CPC (the chromosomal passenger complex) allows its translocalization to the central spindle from the centromeres, where it is located during metaphase. Besides being a structural component of the central spindle itself, CPC also plays a role in the phosphoregulation of other central spindle components, including PRC1 (microtubule-bundling protein required for cytokinesis 1) and MKLP1 (a kinesin motor protein). Originally inhibited by CDK1-mediated phosphorylation, PRC1 is now able to form a homodimer that selectively binds to the interface between antiparallel microtubules, facilitating spatial organization of the microtubules of the central spindle. MKLP1, together with the Rho-family GTPase activating protein CYK-4 (also termed MgcRacGAP), forms the centralspindlin complex. Centralspindlin binds to the central spindle as higher-order clusters. The centralspindlin cluster formation is promoted by phosphorylation of MLKP1 by Aurora B, a component of CPC. In short, the self-assembly of central spindle is initiated through the phosphoregulation of multiple central spindle components by the decline of CDK1 activity, either directly or indirectly, at the metaphase-anaphase transition. The central spindle may have multiple functions in cytokinesis including the control of cleavage furrow positioning, the delivery of membrane vesicles to the cleavage furrow, and the formation of the midbody structure that is required for the final steps of division.<ref name="Morgan-2007">{{cite book|last1=Morgan|first1=David|title=The Cell Cycle|date=2007|publisher=New Science Press|pages=157–173}}</ref>

===Division plane specification===
The second step of animal cell cytokinesis involves division plane specification and cytokinetic furrow formation. Precise positioning of the division plane between the two masses of segregated chromosomes is essential to prevent chromosome loss. Meanwhile, the mechanism by which the spindle determines the division plane in animal cells is perhaps the most enduring mystery in cytokinesis and a matter of intense debate. There exist three hypotheses of furrow induction.<ref name="Morgan-2007"/> The first is the astral stimulation hypothesis, which postulates that astral microtubules from the spindle poles carry a furrow-inducing signal to the cell cortex, where signals from two poles are somehow focused into a ring at the spindle. A second possibility, called the central spindle hypothesis, is that the cleavage furrow is induced by a positive stimulus that originates in the central spindle equator. The central spindle may contribute to the specification of the division plane by promoting concentration and activation of the small GTPase RhoA at the equatorial cortex. A third hypothesis is the astral relaxation hypothesis. It postulates that active actin-myosin bundles are distributed throughout the cell cortex, and inhibition of their contraction near the spindle poles results in a gradient of contractile activity that is highest at the midpoint between poles. In other words, astral microtubules generate a negative signal that increases cortical relaxation close to the poles. Genetic and laser-micromanipulation studies in C. elegans embryos have shown that the spindle sends two redundant signals to the cell cortex, one originating from the central spindle, and a second signal deriving from the spindle aster, suggesting the involvement of multiple mechanisms combined in the positioning of the cleavage furrow. The predominance of one particular signal varies between cell types and organisms. And the multitude and partial redundancy of signals may be required to make the system robust and to increase spatial precision.<ref name="Fededa-2012"/>

===Actin-myosin ring assembly and contraction===
At the cytokinesis [[Biology:Cleavage furrow|cleavage furrow]], it is the [[Biology:Actomyosin ring|actin-myosin contractile ring]] that drives the cleavage process, during which cell membrane and wall grow inward, which eventually pinches the mother cell in two. The key components of this ring are the filamentous protein actin and the motor protein myosin II. The contractile ring assembles equatorially (in the middle of the cell) at the [[Biology:Cell cortex|cell cortex]] (adjacent to the cell membrane). Rho protein family (RhoA protein in mammalian cells) is a key regulator of contractile ring formation and contraction in animal cells.<ref name="Morgan-2007"/> The RhoA pathway promotes assembly of the actin-myosin ring by two main effectors. First, RhoA stimulates nucleation of unbranched actin filaments by activation of Diaphanous-related formins. This local generation of new actin filaments is important for the contractile ring formation.<ref name="Morgan-2007"/> This actin filament formation process also requires a protein called profilin, which binds to actin monomers and helps load them onto the filament end. Second, RhoA promotes myosin II activation by the kinase ROCK, which activates myosin II directly by phosphorylation of the myosin light chain and also inhibits myosin phosphatase by phosphorylation of the phosphatase-targeting subunit MYPT. Besides actin and myosin II, the contractile ring contains the scaffolding protein anillin. Anillin binds to actin, myosin, RhoA, and CYK-4, and thereby links the equatorial cortex with the signals from the central spindle. It also contributes to the linkage of the actin-myosin ring to the plasma membrane. Additionally, anillin generates contractile forces by rectifying thermal fluctuations.<ref>{{cite journal|last1=Kucera| first1=Ondrej| last2=Siahaan| first2=Valerie| last3=Janda| first3=Daniel| last4=Dijkstra| first4=Sietske H| last5=Pilatova| first5=Eliska | last6=Zatecka| first6=Eva | last7=Diez| first7=Stefan | last8=Braun| first8=Marcus | last9=Lansky| first9=Zdenek |date=2021| title=Anillin propels myosin-independent constriction of actin rings | journal=Nature Communications| volume=12| issue=1| page=4595| doi=10.1038/s41467-021-24474-1| pmid=34321459| pmc=8319318| bibcode=2021NatCo..12.4595K}}</ref> Another protein, septin, has also been speculated to serve as a structural scaffold on which the cytokinesis apparatus is organized. Following its assembly, contraction of the actin-myosin ring leads to ingression of the attached plasma membrane, which partitions the cytoplasm into two domains of emerging sister cells. The force for the contractile processes is generated by movements along actin by the motor protein myosin II. Myosin II uses the free energy released when [[Chemistry:Adenosine triphosphate|ATP]] is hydrolyzed to move along these actin filaments, constricting the cell membrane to form a [[Biology:Cleavage furrow|cleavage furrow]]. Continued [[Chemistry:Hydrolysis|hydrolysis]] causes this cleavage furrow to ingress (move inwards), a striking process that is clearly visible through a light microscope.

===Abscission===
The cytokinetic furrow ingresses until a [[Biology:Midbody (cell biology)|midbody structure]] (composed of electron-dense, proteinaceous material) is formed, where the actin-myosin ring has reached a diameter of about 1–2 μm. Most animal cell types remain connected by an intercellular '''cytokinetic bridge''' for up to several hours until they are split by an actin-independent process termed abscission, the last step of cytokinesis.<ref name="Fededa-2012"/><ref>{{Cite web|url=https://www.proteinatlas.org/learn/dictionary/cell/cytokinetic+bridge+4|title=Cytokinetic bridge|website=proteinatlas.org|access-date=28 August 2019|archive-date=28 August 2019|archive-url=https://web.archive.org/web/20190828064449/https://www.proteinatlas.org/learn/dictionary/cell/cytokinetic%2Bbridge%2B4|url-status=dead}}</ref> 

The process of abscission physically cleaves the midbody into two. Abscission proceeds by removal of cytoskeletal structures from the cytokinetic bridge, constriction of the cell cortex, and plasma membrane fission. The intercellular bridge is filled with dense bundles of antiparallel microtubules that derive from the central spindle. These microtubules overlap at the midbody, which is generally thought to be a targeting platform for the abscission machinery. 

The microtubule severing protein [[Medicine:Spastin|spastin]] is largely responsible for the disassembly of microtubule bundles inside the intercellular bridge. Complete cortical constriction also requires removal of the underlying cytoskeletal structures. Actin filament disassembly during late cytokinesis depends on the PKCε–14-3-3 complex, which inactivates RhoA after furrow ingression. Actin disassembly is further controlled by the GTPase Rab35 and its effector, the phosphatidylinositol-4,5-bisphosphate 5-phosphatase OCRL. Understanding the mechanism by which the plasma membrane ultimately splits requires further investigation.

===Timing cytokinesis===

Cytokinesis must be temporally controlled to ensure that it occurs only after sister chromatids separate during the [[Biology:Anaphase|anaphase]] portion of normal proliferative cell divisions. To achieve this, many components of the cytokinesis machinery are highly regulated to ensure that they are able to perform a particular function at only a particular stage of the [[Biology:Cell cycle|cell cycle]].<ref>{{cite journal | vauthors = Mishima M, Pavicic V, Grüneberg U, Nigg EA, Glotzer M | title = Cell cycle regulation of central spindle assembly | journal = Nature | volume = 430 | issue = 7002 | pages = 908–13 | date = August 2004 | pmid = 15282614 | doi = 10.1038/nature02767 | bibcode = 2004Natur.430..908M | s2cid = 4418281 }}</ref><ref>{{cite journal | vauthors = Petronczki M, Glotzer M, Kraut N, Peters JM | title = Polo-like kinase 1 triggers the initiation of cytokinesis in human cells by promoting recruitment of the RhoGEF Ect2 to the central spindle | journal = Dev. Cell | volume = 12 | issue = 5 | pages = 713–25 | date = May 2007 | pmid = 17488623 | doi = 10.1016/j.devcel.2007.03.013 | doi-access = free }}</ref> Cytokinesis happens only after APC binds with CDC20.{{No source|date=May 2022}} This allows for the separation of chromosomes and myosin to work simultaneously.

After cytokinesis, non-kinetochore microtubules reorganize and disappear into a new cytoskeleton as the cell cycle returns to [[Biology:Interphase|interphase]] (see also [[Biology:Cell cycle|cell cycle]]).

== Plant cell ==
Due to the presence of a [[Biology:Cell wall|cell wall]], cytokinesis in plant cells is significantly different from that in animal cells, Rather than forming a contractile ring, plant cells construct a [[Biology:Cell plate|cell plate]] in the middle of the cell. The stages of [[Biology:Cell plate|cell plate]] formation include (1) creation of the [[Biology:Phragmoplast|phragmoplast]], an array of microtubules that guides and supports the formation of the [[Biology:Cell plate|cell plate]]; (2) trafficking of vesicles to the division plane and their fusion to generate a tubular-vesicular network; (3) continued fusion of membrane tubules and their transformation into membrane sheets upon the deposition of [[Chemistry:Callose|callose]], followed by deposition of [[Chemistry:Cellulose|cellulose]] and other [[Biology:Cell wall|cell wall]] components; (4) recycling of excess membrane and other material from the [[Biology:Cell plate|cell plate]]; and (5) fusion with the parental [[Biology:Cell wall|cell wall]]<ref>{{cite journal | vauthors = Otegui M, Staehelin LA | title = Cytokinesis in flowering plants: more than one way to divide a cell | journal = Curr. Opin. Plant Biol. | volume = 3 | issue = 6 | pages = 493–502 | date = December 2000 | pmid = 11074381 | doi = 10.1016/s1369-5266(00)00119-9 }}</ref><ref>{{cite journal | vauthors = Samuels AL, Giddings TH, Staehelin LA | title = Cytokinesis in tobacco BY-2 and root tip cells: a new model of cell plate formation in higher plants | journal = J. Cell Biol. | volume = 130 | issue = 6 | pages = 1345–57 | date = September 1995 | pmid = 7559757 | pmc = 2120572 | doi = 10.1083/jcb.130.6.1345 }}</ref>

The [[Biology:Phragmoplast|phragmoplast]] is assembled from the remnants of the mitotic spindle, and serves as a track for the trafficking of vesicles to the phragmoplast midzone.  These vesicles contain lipids, proteins and carbohydrates needed for the formation of a new cell boundary.  Electron tomographic studies have identified the [[Biology:Golgi apparatus|Golgi apparatus]] as the source of these vesicles,<ref>{{cite journal | vauthors = Otegui MS, Mastronarde DN, Kang BH, Bednarek SY, Staehelin LA | title = Three-dimensional analysis of syncytial-type cell plates during endosperm cellularization visualized by high resolution electron tomography | journal = Plant Cell | volume = 13 | issue = 9 | pages = 2033–51 | date = September 2001 | pmid = 11549762 | pmc = 139450 | doi = 10.1105/tpc.13.9.2033}}</ref><ref>{{cite journal | vauthors = Seguí-Simarro JM, Austin JR, White EA, Staehelin LA | title = Electron tomographic analysis of somatic cell plate formation in meristematic cells of Arabidopsis preserved by high-pressure freezing | journal = Plant Cell | volume = 16 | issue = 4 | pages = 836–56 | date = April 2004 | pmid = 15020749 | pmc = 412860 | doi = 10.1105/tpc.017749 }}</ref> but other studies have suggested that they contain endocytosed material as well.<ref>{{cite journal | vauthors = Baluska F, Liners F, Hlavacka A, Schlicht M, Van Cutsem P, McCurdy DW, Menzel D | title = Cell wall pectins and xyloglucans are internalized into dividing root cells and accumulate within cell plates during cytokinesis | journal = Protoplasma | volume = 225 | issue = 3–4 | pages = 141–55 | date = October 2005 | pmid = 16228896 | doi = 10.1007/s00709-005-0095-5 | s2cid = 11881080 }}</ref><ref>{{cite journal | vauthors = Dhonukshe P, Baluska F, Schlicht M, Hlavacka A, Samaj J, Friml J, Gadella TW | title = Endocytosis of cell surface material mediates cell plate formation during plant cytokinesis | journal = Dev. Cell | volume = 10 | issue = 1 | pages = 137–50 | date = January 2006 | pmid = 16399085 | doi = 10.1016/j.devcel.2005.11.015  | doi-access = free }}</ref>

These tubules then widen and fuse laterally with each other, eventually forming a planar, fenestrated sheet <sup>[8]</sup>.  As the [[Biology:Cell plate|cell plate]] matures, large amounts of membrane material are removed via clathrin-mediated [[Biology:Endocytosis|endocytosis]] <sup>[7]</sup> Eventually, the edges of the cell plate fuse with the parental [[Biology:Plasma membrane|plasma membrane]], often in an asymmetrical fashion,<ref>{{cite journal | vauthors = Cutler SR, Ehrhardt DW | title = Polarized cytokinesis in vacuolate cells of Arabidopsis | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 99 | issue = 5 | pages = 2812–7 | date = March 2002 | pmid = 11880633 | pmc = 122430 | doi = 10.1073/pnas.052712299 | bibcode = 2002PNAS...99.2812C | doi-access = free }}</ref> thus completing cytokinesis.  The remaining fenestrae contain strands of endoplasmic reticulum passing through them, and are thought to be the precursors of plasmodesmata <sup>[8]</sup>.
[[File:Plant and Animal Cell Cytokinesis.svg|thumb|The process of Cytokinesis in a plant cell and an animal cell]]
The construction of the new [[Biology:Cell wall|cell wall]] begins within the lumen of the narrow tubules of the young [[Biology:Cell plate|cell plate]].  The order in which different cell wall components are deposited has been determined largely by immuno-electron microscopy.  The first components to arrive are pectins, [[Biology:Hemicellulose|hemicellulose]]s, and [[Biology:Arabinogalactan protein|arabinogalactan protein]]s carried by the secretory vesicles that fuse to form the cell plate.<ref>{{cite journal|vauthors = Staehelin LA, Moore I|title=The Plant Golgi Apparatus: Structure, Functional Organization and Trafficking Mechanisms|journal=Annual Review of Plant Physiology and Plant Molecular Biology|volume=46|issue=1|year=1995|pages=261–288|issn=1040-2519|doi=10.1146/annurev.pp.46.060195.001401}}</ref>  The next component to be added is [[Chemistry:Callose|callose]], which is polymerized directly at the cell plate by callose synthases.  As the cell plate continues to mature and fuses with the parental plasma membrane, the callose is slowly replaced with [[Chemistry:Cellulose|cellulose]], the primary component of a mature cell wall <sup>[6]</sup>. The [[Biology:Middle lamella|middle lamella]] (a glue-like layer containing pectin) develops from the cell plate, serving to bind the cell walls of adjoining cells together.<ref>{{cite journal |title=On the Origin and Nature of the Middle Lamella |author=Charles E. Allen |journal=Botanical Gazette |volume=32 |issue=1 |date=July 1901 |pages=1–34 |jstor=2464904 |doi=10.1086/328131|s2cid=84936099 }}</ref><ref>{{cite book|vauthors = Evert RF, Eichorn S|title=Esau's Plant Anatomy: Meristems, Cells, and Tissues of the Plant Body: Their Structure, Function, and Development|date=2006-09-18|publisher=John Wiley & Sons|isbn=978-0-470-04737-8}}</ref>

==Forces==

===Animal cells===
Cytokinetic furrow ingression is powered by Type II [[Biology:Myosin ATPase|Myosin ATPase]]. Since Myosins are recruited to the medial region, the contractile forces acting on the cortex resemble a 'purse string' constriction pulling inwards. This leads to the inward constriction. The plasma membrane by virtue of its close association with the cortex via crosslinker proteins <ref>{{cite book|vauthors= Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P|url=https://archive.org/details/molecularbiology0004albe/page/1006/mode/2up|title= "Cross-linking Proteins with Distinct Properties Organize Different Assemblies of Actin Filaments" - Molecular Biology of the Cell, 4th Ed, 2002: Cell|date=2008-06-18|publisher=Garland Science|pages=1006–|isbn=978-0-8153-3218-3}}</ref> To the constriction of the cleavage furrow, the total surface area should be increased by supplying the plasma membrane via exocytosis.<ref>{{cite journal | vauthors = Tanaka M, Fujimoto K, Yumura S | title = Regulation of the Total Cell Surface Area in Dividing Dictyostelium Cells | journal = Front Cell Dev Biol | volume = 8 | page = 238 | date = April 2020 | pmid = 32322581 | pmc = 7156592 | doi = 10.3389/fcell.2020.00238 | doi-access = free }}</ref>

Theoretical models show that symmetric constriction requires both lateral stabilization and constriction forces.<ref>{{Cite journal |last1=Beltrán-Heredia |first1=Elena |last2=Monroy |first2=Francisco |last3=Cao-García |first3=Francisco J. |date=2019-11-21 |title=Mechanical conditions for stable symmetric cell constriction |url=https://link.aps.org/doi/10.1103/PhysRevE.100.052408 |journal=Physical Review E |volume=100 |issue=5 |pages=052408 |doi=10.1103/PhysRevE.100.052408|pmid=31869912 |bibcode=2019PhRvE.100e2408B |hdl=10261/205685 |hdl-access=free }}</ref> Reduction of external pressure and of surface tension (by membrane trafficking) reduce the required stabilization and constriction forces. 

==Proteins involved in cytokinesis==

CEP55 is a mitotic phosphoprotein that plays a key role in cytokinesis, the final stage of cell division.<ref>{{cite journal | vauthors = van der Horst A, Simmons J, Khanna KK | title = Cep55 stabilization is required for normal execution of cytokinesis | journal = Cell Cycle | volume = 8 | issue = 22 | pages = 3742–9 |date=November 2009 | pmid = 19855176 | doi = 10.4161/cc.8.22.10047 | doi-access = free }}</ref><ref>{{cite journal |author=Behnam Rashidieh |author2=Belal Shohayeb |author3=Amanda Louise Bain |author4=Patrick R. J. Fortuna |author5=Debottam Sinha |author6=Andrew Burgess |author7=Richard Mills |author8=Rachael C. Adams |author9=J. Alejandro Lopez |author10=Peter Blumbergs |author11=John Finnie |author12=Murugan Kalimutho |author13=Michael Piper |author14=James Edward Hudson |author15=Dominic C. H. Ng |author16=Kum Kum Khanna
 | title = Cep55 regulation of PI3K/Akt signaling is required for neocortical development and ciliogenesis | journal = PLOS Genetics |date=October 2021 | volume = 17 | issue = 10 | pages = e1009334 | pmid = 34710087 | doi = 10.1371/journal.pgen.1009334 | doi-access = free |pmc=8577787 }}</ref>
==Clinical significance==
In some cases, a cell may divide its genetic material and grow in size, but fail to undergo cytokinesis. This results in larger cells with more than one nucleus. Usually this is an unwanted aberration and can be a sign of cancerous cells.<ref>{{CC-notice|cc=by4|url=https://openstax.org/books/anatomy-and-physiology/pages/3-5-cell-growth-and-division}} {{cite book|last1=Betts|first1=J Gordon|last2=Desaix|first2=Peter|last3=Johnson|first3=Eddie|last4=Johnson|first4=Jody E|last5=Korol|first5=Oksana|last6=Kruse|first6=Dean|last7=Poe|first7=Brandon|last8=Wise|first8=James|last9=Womble|first9=Mark D|last10=Young|first10=Kelly A|title=Anatomy & Physiology|location=Houston|publisher=OpenStax CNX|isbn=978-1-947172-04-3|date=June 8, 2023|at=3.5 Cell Growth and Division}}</ref>

==See also==
* {{annotated link|Biology:Telophase}}
* {{annotated link|Biology:Prophase}}
* {{annotated link|Biology:Anaphase}}
* {{annotated link|Biology:Metaphase}}
* {{annotated link|Biology:Mitosis}}
* {{annotated link|Biology:Cell theory}}
* {{annotated link|Biology:Cytoskeleton}}

==References==
{{reflist}}

== Further reading ==
*''The Molecular Requirements for Cytokinesis'' by M. Glotzer (2005), Science 307, 1735
*"Animal Cytokinesis: from parts list to mechanism" by Eggert, U.S., Mitchison, T.J., Field, C.M. (2006), Annual Review of Cell Biology 75, 543-66
*''Campbell Biology'' (2010), 580-582
*[https://web.archive.org/web/20100622024242/http://www.illuminatedcell.com/celldiv.html More description and nice images of cell division in plants, with a focus on fluorescence microscopy]
*{{cite journal |title = Cytokinesis in Prokaryotes and Eukaryotes: Common Principles and Different Solutions | pmc=99029 | pmid=11381104 | doi=10.1128/MMBR.65.2.319-333.2001 | volume=65 | issue=2 | date=June 2001 | journal=Microbiol. Mol. Biol. Rev. | pages=319–33 | author=Nanninga N}}

{{Cell cycle}}

[[Category:Cell cycle]]
[[Category:Mitosis]]
[[Category:Meiosis]]

{{Sourceattribution|Cytokinesis}}