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J Cell Biol. 2018 Dec 3;217(12):4230-4252. doi: 10.1083/jcb.201806161. Epub 2018 Oct 1.

Excitable RhoA dynamics drive pulsed contractions in the early C. elegans embryo.

Author information

1
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL.
2
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL francois.robin@upmc.fr.
3
Biophysics Program, University of Chicago, Chicago, IL.
4
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL emunro@uchicago.edu.
5
Institute for Biophysical Dynamics, University of Chicago, Chicago, IL.

Abstract

Pulsed actomyosin contractility underlies diverse modes of tissue morphogenesis, but the underlying mechanisms remain poorly understood. Here, we combined quantitative imaging with genetic perturbations to identify a core mechanism for pulsed contractility in early Caenorhabditis elegans embryos. We show that pulsed accumulation of actomyosin is governed by local control of assembly and disassembly downstream of RhoA. Pulsed activation and inactivation of RhoA precede, respectively, the accumulation and disappearance of actomyosin and persist in the absence of Myosin II. We find that fast (likely indirect) autoactivation of RhoA drives pulse initiation, while delayed, F-actin-dependent accumulation of the RhoA GTPase-activating proteins RGA-3/4 provides negative feedback to terminate each pulse. A mathematical model, constrained by our data, suggests that this combination of feedbacks is tuned to generate locally excitable RhoA dynamics. We propose that excitable RhoA dynamics are a common driver for pulsed contractility that can be tuned or coupled differently to actomyosin dynamics to produce a diversity of morphogenetic outcomes.

PMID:
30275107
PMCID:
PMC6279378
DOI:
10.1083/jcb.201806161
[Indexed for MEDLINE]
Free PMC Article

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