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Actin turnover maintains actin filament homeostasis during cytokinetic ring contraction

Research output: Contribution to journalArticle

Ting Gang Chew, Junqi Huang, Saravanan Palani, Ruth Sommese, Anton Kamnev, Tomoyuki Hatano, Ying Gu, Snezhana Oliferenko, Sivaraj Sivaramakrishnan, Mohan K. Balasubramanian

Original languageEnglish
Pages (from-to)2657-2667
Number of pages11
JournalJournal of Cell Biology
Issue number9
Publication statusPublished - 1 Sep 2017

King's Authors


Cytokinesis in many eukaryotes involves a tension-generating actomyosin-based contractile ring. Many components of actomyosin rings turn over during contraction, although the significance of this turnover has remained enigmatic. Here, using Schizosaccharomyces japonicus, we investigate the role of turnover of actin and myosin II in its contraction. Actomyosin ring components self-organize into ~1-μm-spaced clusters instead of undergoing full-ring contraction in the absence of continuous actin polymerization. This effect is reversed when actin filaments are stabilized. We tested the idea that the function of turnover is to ensure actin filament homeostasis in a synthetic system, in which we abolished turnover by fixing rings in cell ghosts with formaldehyde. We found that these rings contracted fully upon exogenous addition of a vertebrate myosin. We conclude that actin turnover is required to maintain actin filament homeostasis during ring contraction and that the requirement for turnover can be bypassed if homeostasis is achieved artificially.

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