# Dynamics and regulation of actomyosin contractility in the C. elegans embryo

> **NIH NIH R01** · UNIVERSITY OF CHICAGO · 2020 · $326,268

## Abstract

Abstract
The broad goal of this study is to elucidate basic mechanisms by which embryonic cells exert
rapid spatiotemporal control over subcellular organization and force production to move, change
shape, divide and execute tissue morphogenesis. Cells do this in part by patterning intracellular
signals that regulate assembly and force production by the actomyosin cytoskeleton. At same
time, cytoskeletal dynamics and contractility feed back to modulate the distributions and
activities of their upstream regulators. A fundamental challenge is to understanding how robust
spatiotemporal control of cell behavior emerges from dynamic interplay of intracellular signaling,
cytoskeletal dynamics and cytomechanics, and how failures in this process produce
developmental defects and human disease.
We will address this challenge using the C. elegans embryo as a model system to study two
fundamental, widespread and highly conserved forms of mechanochemical patterning: The first
is pulsed actomyosin contractility in which the episodic assembly, contraction and disassembly
of contractile networks drive transient deformations of the cell surface to control cell shape
change, cortical flow and tissue deformation. The second is dynamic formation and stabilization
of cortical polarity through interactions among conserved PAR polarity proteins, Rho family
GTPases and the actomyosin cytoskeleton. C. elegans embryos provide a unique opportunity to
study these processes at the surface of single large cells in vivo using quantitative microscopy
and well-developed tools for genetic manipulation. Building on our previous studies, we will use
a tightly integrated combination of quantitative imaging, experimental manipulations, and
predictive computer simulations to address the following questions:
1) How do tunable spatiotemporal dynamics of pulsed contractility emerge from dynamic
 coupling of RhoA signaling and actomyosin contractility?
2) How are stable boundaries between polarized domains maintained in the face of
 continuous exchange and diffusion, through dynamic clustering, positive feedback and
 mutual antagonism of polarity proteins?
3) How is the polarity boundary maintained in the face of persistent contractile asymmetries
 through feedback mechanisms that couple PAR proteins, small GTPases and
 actomyosin contractility?
Because the molecular players involved in these processes are highly conserved, our work will
have direct relevance for understanding cell polarity and spatiotemporal control of actomyosin
contractility in many other contexts, both in health and disease.

## Key facts

- **NIH application ID:** 9968364
- **Project number:** 5R01GM098441-09
- **Recipient organization:** UNIVERSITY OF CHICAGO
- **Principal Investigator:** Edwin Marshall Munro
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $326,268
- **Award type:** 5
- **Project period:** 2011-09-20 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9968364

## Citation

> US National Institutes of Health, RePORTER application 9968364, Dynamics and regulation of actomyosin contractility in the C. elegans embryo (5R01GM098441-09). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9968364. Licensed CC0.

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