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


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.

SUBMITTER: Garbett D 

PROVIDER: S-EPMC7511357 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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

Garbett Damien D   Bisaria Anjali A   Yang Changsong C   McCarthy Dannielle G DG   Hayer Arnold A   Moerner W E WE   Svitkina Tatyana M TM   Meyer Tobias T  

Nature communications 20200923 1


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 protrusion  ...[more]

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