Cytokinetic actomyosin ring disassembly occurs through a novel mechanism in which the increased ring curvature, generated through contraction, itself promotes the disassembly process.

Functional molecular analysis of cytokinesis in Caenorhabditis elegans four-cell embryos reveals cell-type-specific variation in the fundamental dependence on a robust f-actin cytoskeleton for successful cell division, mediated by both cell-intrinsic and -extrinsic pathways.

Activation of the key regulator of cytokinesis, RhoA, involves an unexpected contribution by a RhoGAP domain.

ULK3 is a kinase in the abscission checkpoint that temporarily inactivates ESCRT-III proteins via phosphorylation, which is required to delay cytokinesis in response to defects in mitosis.

Asymmetric tension increase along the cell equator promotes self-organization of actomyosin into a partially aligned network during cytokinetic cleavage furrow ingression of vertebrate cells.

Lagging chromosomes in anaphase inhibits cytokinesis in plant cells.

MT plus-end-mediated recruitment of a cortical pool of ECT2 trigger RhoA activation upon contact, which results in localized contractility during cytokinesis.

Aneuploidy can cause chromosome mis-segregation and specific cellular phenotypes driven by expression of genes on the extra chromosome.

SNARE proteins are delivered as complexes already from the endoplasmic reticulum along the secretory pathway to the cell division plane to mediate the formation of the partitioning membrane by vesicle fusion.

Positive feedback between contractile ring myosin and compression-driven cortical flow can explain the exponential accumulation of contractile ring components and constriction rate acceleration that ensures timely cell separation during cytokinesis.