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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Garbett D,Bisaria A,Yang C,McCarthy DG,Hayer A,Moerner WE,Svitkina TM,Meyer T

doi

10.1038/s41467-020-18586-3

subject

Has Abstract

pub_date

2020-09-23 00:00:00

pages

4818

issue

1

issn

2041-1723

pii

10.1038/s41467-020-18586-3

journal_volume

11

pub_type

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