Myosin II governs intracellular pressure and traction by distinct tropomyosin-dependent mechanisms

Two-dimensional (2D) substrate rigidity promotes myosin II activity to increase traction force in a process negatively regulated by tropomyosin (Tpm) 2.1. We recently discovered that actomyosin contractility can increase intracellular pressure and switch tumor cells from low-pressure lamellipodia to...

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Published in:Molecular biology of the cell Vol. 30; no. 10; pp. mbcE18060355 - 1181
Main Authors: Sao, Kimheak, Jones, Tia M, Doyle, Andrew D, Maity, Debonil, Schevzov, Galina, Chen, Yun, Gunning, Peter W, Petrie, Ryan J
Format: Journal Article
Language:English
Published: United States The American Society for Cell Biology 01-05-2019
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Summary:Two-dimensional (2D) substrate rigidity promotes myosin II activity to increase traction force in a process negatively regulated by tropomyosin (Tpm) 2.1. We recently discovered that actomyosin contractility can increase intracellular pressure and switch tumor cells from low-pressure lamellipodia to high-pressure lobopodial protrusions during 3D migration. However, it remains unclear whether these myosin II-generated cellular forces are produced simultaneously, and by the same molecular machinery. Here we identify Tpm 1.6 as a positive regulator of intracellular pressure and confirm that Tpm 2.1 is a negative regulator of traction force. We find that Tpm 1.6 and 2.1 can control intracellular pressure and traction independently, suggesting these myosin II-dependent forces are generated by distinct mechanisms. Further, these tropomyosin-regulated mechanisms can be integrated to control complex cell behaviors on 2D and in 3D environments.
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The authors declare no competing financial interests.
ISSN:1059-1524
1939-4586
DOI:10.1091/mbc.E18-06-0355