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Mol Biol Cell. 2011 Oct;22(20):3768-78. doi: 10.1091/mbc.E10-12-0952. Epub 2011 Aug 17.

Citron kinase controls abscission through RhoA and anillin.

Author information

1
Department of Genetics, Biology, and Biochemistry, Molecular Biotechnology Center, University of Turin, 10126 Turin, Italy.

Abstract

The small GTPase RhoA plays a crucial role in the different stages of cytokinesis, including contractile ring formation, cleavage furrow ingression, and midbody abscission. Citron kinase (CIT-K), a protein required for cytokinesis and conserved from insects to mammals, is currently considered a cytokinesis-specific effector of active RhoA. In agreement with previous observations, we show here that, as in Drosophila cells, CIT-K is specifically required for abscission in mammalian cells. However, in contrast with the current view, we provide evidence that CIT-K is an upstream regulator rather than a downstream effector of RhoA during late cytokinesis. In addition, we show that CIT-K is capable of physically and functionally interacting with the actin-binding protein anillin. Active RhoA and anillin are displaced from the midbody in CIT-K-depleted cells, while only anillin, but not CIT-K, is affected if RhoA is inactivated in late cytokinesis. The overexpression of CIT-K and of anillin leads to abscission delay. However, the delay produced by CIT-K overexpression can be reversed by RhoA inactivation, while the delay produced by anillin overexpression is RhoA-independent. Altogether, these results indicate that CIT-K is a crucial abscission regulator that may promote midbody stability through active RhoA and anillin.

PMID:
21849473
PMCID:
PMC3192857
DOI:
10.1091/mbc.E10-12-0952
[Indexed for MEDLINE]
Free PMC Article

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