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.
Bibliographical noteFunding Information:
This work was supported by Wellcome Trust Senior Investigator Awards to M.K. Balasubramanian (WT101885MA) and S. Olife-renko (103741/Z/14/Z). For this work, M.K. Balasubramanian was also supported by a Royal Society Wolfson Merit Award and an European Research Council Advanced Grant (ERC-2014-ADG no. 671083). The authors declare no competing financial interests.
© 2017 Chew et al.