Format

Send to

Choose Destination
Nat Commun. 2017 Jun 12;8:15817. doi: 10.1038/ncomms15817.

Optogenetic control of RhoA reveals zyxin-mediated elasticity of stress fibres.

Author information

1
Institute for Biophysical Dynamics, University of Chicago, Chicago, Illinois 606037, USA.
2
James Franck Institute, University of Chicago, Chicago, Illinois 606037, USA.
3
Department of Physics, University of Chicago, Chicago, Illinois 606037, USA.
4
Department of Physics &Astronomy, University of Rochester, Rochester, New York 14627, USA.
5
Department of Biology, University of Rochester, Rochester, New York 14627, USA.
6
Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, Illinois 60637, USA.
7
Institute for Theoretical Physics and BioQuant, Heidelberg University, Heidelberg 69120, Germany.

Abstract

Cytoskeletal mechanics regulates cell morphodynamics and many physiological processes. While contractility is known to be largely RhoA-dependent, the process by which localized biochemical signals are translated into cell-level responses is poorly understood. Here we combine optogenetic control of RhoA, live-cell imaging and traction force microscopy to investigate the dynamics of actomyosin-based force generation. Local activation of RhoA not only stimulates local recruitment of actin and myosin but also increased traction forces that rapidly propagate across the cell via stress fibres and drive increased actin flow. Surprisingly, this flow reverses direction when local RhoA activation stops. We identify zyxin as a regulator of stress fibre mechanics, as stress fibres are fluid-like without flow reversal in its absence. Using a physical model, we demonstrate that stress fibres behave elastic-like, even at timescales exceeding turnover of constituent proteins. Such molecular control of actin mechanics likely plays critical roles in regulating morphodynamic events.

PMID:
28604737
PMCID:
PMC5477492
DOI:
10.1038/ncomms15817
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center