T-Plastin reinforces membrane protrusions to bridge matrix gaps during cell migration

Damien Garbett (), Anjali Bisaria, Changsong Yang, Dannielle G. McCarthy, Arnold Hayer, W. E. Moerner, Tatyana M. Svitkina and Tobias Meyer ()
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Damien Garbett: Stanford University
Anjali Bisaria: Stanford University
Changsong Yang: University of Pennsylvania
Dannielle G. McCarthy: Stanford University
Arnold Hayer: Stanford University
W. E. Moerner: Stanford University
Tatyana M. Svitkina: University of Pennsylvania
Tobias Meyer: Stanford University

Nature Communications, 2020, vol. 11, issue 1, 1-18

Abstract: Abstract Migrating cells move across diverse assemblies of extracellular matrix (ECM) that can be separated by micron-scale gaps. For membranes to protrude and reattach across a gap, actin filaments, which are relatively weak as single filaments, must polymerize outward from adhesion sites to push membranes towards distant sites of new adhesion. Here, using micropatterned ECMs, we identify T-Plastin, one of the most ancient actin bundling proteins, as an actin stabilizer that promotes membrane protrusions and enables bridging of ECM gaps. We show that T-Plastin widens and lengthens protrusions and is specifically enriched in active protrusions where F-actin is devoid of non-muscle myosin II activity. Together, our study uncovers critical roles of the actin bundler T-Plastin to promote protrusions and migration when adhesion is spatially-gapped.

Date: 2020
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DOI: 10.1038/s41467-020-18586-3

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