Optogenetic control of RhoA reveals zyxin-mediated elasticity of stress fibres
Patrick W. Oakes,
Elizabeth Wagner,
Christoph A. Brand,
Dimitri Probst,
Marco Linke,
Ulrich S. Schwarz (),
Michael Glotzer () and
Margaret L. Gardel ()
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Patrick W. Oakes: Institute for Biophysical Dynamics, University of Chicago
Elizabeth Wagner: University of Chicago
Christoph A. Brand: Institute for Theoretical Physics and BioQuant, Heidelberg University
Dimitri Probst: Institute for Theoretical Physics and BioQuant, Heidelberg University
Marco Linke: Institute for Theoretical Physics and BioQuant, Heidelberg University
Ulrich S. Schwarz: Institute for Theoretical Physics and BioQuant, Heidelberg University
Michael Glotzer: University of Chicago
Margaret L. Gardel: Institute for Biophysical Dynamics, University of Chicago
Nature Communications, 2017, vol. 8, issue 1, 1-12
Abstract:
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.
Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15817
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DOI: 10.1038/ncomms15817
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