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Published July 5, 2004 | Published + Supplemental Material
Journal Article Open

Mutations in sticky lead to defective organization of the contractile ring during cytokinesis and are enhanced by Rho and suppressed by Rac

Abstract

The contractile ring is a highly dynamic structure, but how this dynamism is accomplished remains unclear. Here, we report the identification and analysis of a novel Drosophila gene, sticky (sti), essential for cytokinesis in all fly proliferating tissues. sti encodes the Drosophila orthologue of the mammalian Citron kinase. RNA interference–mediated silencing of sti in cultured cells causes them to become multinucleate. Components of the contractile ring and central spindle are recruited normally in such STICKY-depleted cells that nevertheless display asymmetric furrowing and aberrant blebbing. Together with an unusual distribution of F-actin and Anillin, these phenotypes are consistent with defective organization of the contractile ring. sti shows opposite genetic interactions with Rho and Rac genes suggesting that these GTPases antagonistically regulate STICKY functions. Similar genetic evidence indicates that RacGAP50C inhibits Rac during cytokinesis. We discuss that antagonism between Rho and Rac pathways may control contractile ring dynamics during cytokinesis.

Additional Information

© 2004 The Rockefeller University Press. After the Initial Publication Period, RUP will grant to the public the non-exclusive right to copy, distribute, or display the Article under a Creative Commons Attribution-Noncommercial-Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode, or updates thereof. Submitted: 29 February 2004. Accepted: 24 May 2004. We are very grateful to A.T. Carpenter for her help with the genetic mapping of sti and for the sti2 and sti3 alleles, and to G. Kingshott for injections. We also thank R. Karess, C. Field, E. Giordano, R. Saint, and the Bloomington stock center for reagents. This work was supported by grants from the Cancer Research-UK, UK Medical Research Council, and European Union to D.M. Glover; and by an MRC Cambridge Drosophila Co-operative Group grant. The online version of this article contains supplemental material.

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