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EnglishThe 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) is a conserved protein required for cytokinesis from insects to mammals, currently considered a cytokinesis-specific effector of active RhoA. In agreement with previous suggestions, we show here that, as in the case of Drosophila cells, even in mammalian cells CIT-K is specifically required for abscission. However, in contrast with the current view, we provide evidence that, during late cytokinesis, CIT-K is an upstream regulator rather than a downstream effector of RhoA. In addition, we show that CIT-K is capable to physically and functionally interact with the actin-binding protein Anillin. Active RhoA and the 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 reverted 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.
| Titolo: | Citron kinase controls abscission through RhoA and Anillin. | |
| Autori Riconosciuti: | ||
| Autori: | Gai M; Camera P; Dema A; Bianchi F; Berto G; Scarpa E; Germena G; Di Cunto F | |
| Data di pubblicazione: | 2011 | |
| 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) is a conserved protein required for cytokinesis from insects to mammals, currently considered a cytokinesis-specific effector of active RhoA. In agreement with previous suggestions, we show here that, as in the case of Drosophila cells, even in mammalian cells CIT-K is specifically required for abscission. However, in contrast with the current view, we provide evidence that, during late cytokinesis, CIT-K is an upstream regulator rather than a downstream effector of RhoA. In addition, we show that CIT-K is capable to physically and functionally interact with the actin-binding protein Anillin. Active RhoA and the 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 reverted 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. | |
| Volume: | 22 | |
| Fascicolo: | 20 | |
| Pagina iniziale: | 3768 | |
| Pagina finale: | 3778 | |
| Digital Object Identifier (DOI): | 10.1091/mbc.E10-12-0952 | |
| URL: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3192857/ | |
| Rivista: | MOLECULAR BIOLOGY OF THE CELL | |
| Appare nelle tipologie: | 03A-Articolo su Rivista |
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