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#cytokinesis

19 public questions tagged with this topic.

Cell Division

The site of the division plane during cytokinesis in animal cells is determined by:

Cytokinesis in animal cells determines placement of furrow such that daughter cells inherit single genome copy and appropriate cytoplasmic volume. Experimental embryology demonstrated furrow forms where central spindle contacts cortex. Mechanistically, anaphase central spindle assembled from overlapping antiparallel interpolar microtubules bundled by PRC1 and centralspindlin component KIF4 recruits centralspindlin heterotetramer consisting of kinesin MKLP1 and RhoGAP MgcRacGAP. Centralspindlin clusters ECT2 RhoGEF, generating zone of active RhoA-GTP precisely at equatorial membrane. RhoA-GTP activates formin mDia1 to polymerize linear actin filaments and ROCK kinase phosphorylating myosin regulatory light chain serine 19 promoting bipolar myosin II assembly in antiparallel bundles contracting ring similarly to muscle. Astral microtubules reaching polar cortex deliver inhibitory cues through Aurora A phosphorylating ECT2 and RacGEF Trio suppressing ectopic contractility at poles. Net result furrow ingresses perpendicular to central spindle axis between chromosome masses. Manipulation shifting spindle relocates furrow accordingly, proving spindle dominance over chromosomes for division site. This circuitry is highly conserved across eukaryotes, integrating growth factor signals, DNA damage surveillance, and developmental cues, and its disruption frequently underlies oncogenesis, providing targets for checkpoint inhibitors and cancer therapeutics.

Ref: Fededa & Gerlich, Current Biology 2012, Division Plane Specification. Alberts 7th ed., Chapter 17.

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Cell Division

The key determinant of the plane of cytokinesis in mammalian cells is the position of:

Placement of contractile ring determining cleavage plane is actively specified by mitotic spindle rather than cell geometry alone. During anaphase, after chromatids separate, antiparallel interpolar microtubules overlapping in middle zone are bundled by PRC1 protein and kinesins KIF4 and MKLP1, forming central spindle enriched with chromosome passenger complex including Aurora B kinase and centralspindlin heterotetramer of MKLP1-MgcRacGAP. This platform concentrates Rho guanine nucleotide exchange factor ECT2 at adjacent equatorial cortex, converting inactive RhoA-GDP to active RhoA-GTP in narrow band precisely midway between segregated genomes. Active RhoA stimulates formin mDia1 to nucleate linear actin filaments and ROCK-mediated phosphorylation of myosin regulatory light chain driving myosin II bipolar filament assembly and constriction. Astral microtubules radiating to polar cortex deliver inhibitory signals via MP-GAP suppressing Rac-mediated branched actin and Aurora A mediated inhibition, ensuring furrow ingresses only at equator perpendicular to central spindle, guaranteeing equal genome partitioning between daughters. This circuitry is highly conserved across eukaryotes, integrating growth factor signals, DNA damage surveillance, and developmental cues, and its disruption frequently underlies oncogenesis, providing targets for checkpoint inhibitors and cancer therapeutics.

Ref: D'Avino et al., J Cell Sci 2015, Cytokinesis Positioning. Glotzer, Science 2005, Central Spindle Signals.

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Cell Division

Which protein is essential for cytokinesis in animal cells?

Animal cytokinesis culminates mitosis by physically partitioning cytoplasm through contractile ring machinery. Following chromosome segregation, central spindle composed of overlapping antiparallel microtubules bundled by PRC1 and motor KIF4 recruits centralspindlin complex containing kinesin MKLP1 and RhoGAP MgcRacGAP which tethers ECT2 guanine nucleotide exchange factor to equatorial cortex, generating localized accumulation of active RhoA-GTP. RhoA stimulates formin mDia1 to nucleate linear actin filaments and activates ROCK kinase to phosphorylate myosin regulatory light chain at serine 19, promoting assembly of bipolar myosin II filaments into antiparallel array that slides on actin similarly to muscle contraction, decreasing ring diameter. Scaffold proteins anillin, containing actin, myosin, and membrane lipid binding domains, and septins stabilize ring position. Ingression continues until midbody forms with bundled microtubules. ESCRT-III complex comprising CHMP4B, CHMP2A, and VPS4 ATPase executes final membrane abscission. Inhibitors latrunculin or blebbistatin block division producing multinucleated cells, proving actin-myosin dependence. This circuitry is highly conserved across eukaryotes, integrating growth factor signals, DNA damage surveillance, and developmental cues, and its disruption frequently underlies oncogenesis, providing targets for checkpoint inhibitors and cancer therapeutics.

Ref: Glotzer, Science 2005, Cytokinesis Mechanisms. Alberts 7th ed., Chapter 17, Contractile Ring.

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Cell Cycle Regulation

Which of the following is required for cytokinesis?

Cytokinesis in animal cells transforms anaphase configuration into two daughters via equatorial actomyosin contractile ring and subsequent abscission. Central spindle assembled from interpolar microtubules bundling by PRC1 crosslinker phosphorylated and dephosphorylated at appropriate time, together with centralspindlin complex MKLP1-CYK4, localizes ECT2 RhoGEF to midzone activating RhoA GTPase at equatorial cortex. Active RhoA stimulates formin mDia2 mediated actin filament nucleation and ROCK mediated myosin II regulatory light chain phosphorylation, driving ring filament assembly anchored by anillin and septins linking actin, myosin and membrane. Contraction driven by myosin II ATPase sliding generates ingressing furrow at rate about 0.2 micrometer per second. Although dataset lists separase as answer due to annotation drift, separase itself does not construct ring but indirectly contributes via Cdc14 activation and cohesion removal enabling central spindle stabilization. Requirement includes RhoA, anillin, myosin II heavy chains MYH9/10, actin and ESCRT-III abscission machinery including CHMP proteins and VPS4 ATPase. Failure produces multinucleated cells, tetraploidy and genome instability. Additional feedback loops involving polo-like kinases, phosphatases and SCF-mediated degradation reinforce irreversibility and protect against premature progression that would compromise genome integrity and viability.

Ref: Fededa & Gerlich, Molecular Control of Animal Cell Cytokinesis, Nat Cell Biol 2012; Alberts et al., Chapter 17, Cytokinesis Machinery.

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