*For correspondence: renatkh@gmail.com (RNK); koegema@ucsd.edu (KO) Competing interests: The authors declare that no competing interests exist. Funding: See page 28 Received: 20 February 2018 Accepted: 01 July 2018 Published: 02 July 2018 Reviewing editor: Mohan K Balasubramanian, University of Warwick, United Kingdom Copyright Khaliullin et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited. A positive-feedback-based mechanism for constriction rate acceleration during cytokinesis in Caenorhabditis elegans Renat N Khaliullin 1 *, Rebecca A Green 1 , Linda Z Shi 2 , J Sebastian Gomez-Cavazos 1 , Michael W Berns 2 , Arshad Desai 1 , Karen Oegema 1 * 1 Department of Cellular and Molecular Medicine, Ludwig Institute for Cancer Research, University of California, San Diego, San Diego, United States; 2 Department of Bioengineering and Institute of Engineering in Medicine, University of California, San Diego, San Diego, United States Abstract To ensure timely cytokinesis, the equatorial actomyosin contractile ring constricts at a relatively constant rate despite its progressively decreasing size. Thus, the per-unit-length constriction rate increases as ring perimeter decreases. To understand this acceleration, we monitored cortical surface and ring component dynamics during the first cytokinesis of the Caenorhabditis elegans embryo. We found that, per unit length, the amount of ring components (myosin, anillin) and the constriction rate increase with parallel exponential kinetics. Quantitative analysis of cortical flow indicated that the cortex within the ring is compressed along the axis perpendicular to the ring, and the per-unit-length rate of cortical compression increases during constriction in proportion to ring myosin. We propose that positive feedback between ring myosin and compression-driven flow of cortex into the ring drives an exponential increase in the per-unit- length amount of ring myosin to maintain a high ring constriction rate and support this proposal with an analytical mathematical model. DOI: https://doi.org/10.7554/eLife.36073.001 Introduction During cytokinesis in animal cells, constriction of an equatorial actomyosin ring cinches the mother cell surface to generate a dumbbell-shaped structure with an intercellular bridge that connects the two daughter cells (Fededa and Gerlich, 2012; Green et al., 2012). This cellular shape change is brought about by a cortical contractile ring that assembles around the cell equator following chro- mosome segregation in anaphase. To ensure that each cell inherits a single genomic complement, contractile ring assembly is directed by the small GTPase RhoA. RhoA is activated in an equatorial zone (the ‘Rho zone’) in response to signaling by the anaphase spindle (Green et al., 2012; Jordan and Canman, 2012; Piekny et al., 2005) and patterns the equatorial cortex by recruiting contractile ring components from the cytoplasm (Vale et al., 2009; Yumura, 2001; Zhou and Wang, 2008). RhoA activates Rho kinase, which promotes the assembly and recruitment of myosin II (Matsumura et al., 2011) and the cytokinesis formin that assembles the long actin filaments that make up the ring (Otomo et al., 2005). Contractile rings also contain membrane-associated septin filaments (Bridges and Gladfelter, 2015) and the filament cross linker anillin (D’Avino, 2009; Piekny and Maddox, 2010). Recent work in the Caenorhabditis elegans embryo suggests that the equatorial cortex is compressed along the pole-to-pole axis after this initial patterning, leading to the alignment of actin filament bundles as the ring forms (Reymann et al., 2016). After its assembly, the ring begins to constrict in the around-the-ring direction. Constriction is thought to be coupled to Khaliullin et al. eLife 2018;7:e36073. DOI: https://doi.org/10.7554/eLife.36073 1 of 32 RESEARCH ARTICLE