Cytokinesis

The word "cytokinesis" () uses combining forms of cyto- + kine- + -sis, Neo-Latin from Classical Latin and Ancient Greek, reflecting "cell" and kinesis ("motion, movement"). It was coined by Charles Otis Whitman in 1887. Origin of this term is from Greek (', a hollow), Latin derivative ' (cellular), Greek ('''', movement). == Animal cell ==

and cytokinesis In an animal cell cytokinesis begins shortly after the onset of sister chromatid separation in the anaphase of mitosis. The process can be divided to the following distinct steps: anaphase spindle reorganization, division plane specification, cytokinetic ring assembly and contraction, and abscission. 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 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, D. melanogaster and C. elegans require the central spindle in order to efficiently undergo cytokinesis, although the specific 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 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. 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. 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 ATP is hydrolyzed to move along these actin filaments, constricting the cell membrane to form a cleavage furrow. Continued 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 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. 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 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. The final step of abscission is controlled by the recruitment and polymerization of the endosomal sorting complex required for transport III (ESCRT-III), which serves to physically constrict and separate the plasma membrane of the two adjoined daughter cells. Timing cytokinesis Cytokinesis must be temporally controlled to ensure that it occurs only after sister chromatids separate during the 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 cell cycle. Cytokinesis happens only after APC binds with CDC20. 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 interphase (see also cell cycle). == Plant cell ==

Due to the presence of a cell wall, cytokinesis in plant cells is significantly different from that in animal cells, Rather than forming a contractile ring, plant cells construct a cell plate in the middle of the cell. The stages of cell plate formation include (1) creation of the phragmoplast, an array of microtubules that guides and supports the formation of the 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 callose, followed by deposition of cellulose and other cell wall components; (4) recycling of excess membrane and other material from the cell plate; and (5) fusion with the parental cell wall The 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 Golgi apparatus as the source of these vesicles, but other studies have suggested that they contain endocytosed material as well. These tubules then widen and fuse laterally with each other, eventually forming a planar, fenestrated sheet [8]. As the cell plate matures, large amounts of membrane material are removed via clathrin-mediated endocytosis [7] Eventually, the edges of the cell plate fuse with the parental plasma membrane, often in an asymmetrical fashion, thus completing cytokinesis. The remaining fenestrae contain strands of endoplasmic reticulum passing through them, and are thought to be the precursors of plasmodesmata [8]. The construction of the new cell wall begins within the lumen of the narrow tubules of the young 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, hemicelluloses, and arabinogalactan proteins carried by the secretory vesicles that fuse to form the cell plate. The next component to be added is 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 cellulose, the primary component of a mature cell wall [6]. The middle lamella (a glue-like layer containing pectin) develops from the cell plate, serving to bind the cell walls of adjoining cells together. ==Forces==

Animal cells Cytokinetic furrow ingression is powered by Type II 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 To the constriction of the cleavage furrow, the total surface area should be increased by supplying the plasma membrane via exocytosis. Theoretical models show that symmetric constriction requires both lateral stabilization and constriction forces. 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. ==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. ==See also==