T-Plastin reinforces membrane protrusions to bridge matrix gaps during cell migration. Academic Article uri icon

Overview

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.

publication date

  • September 23, 2020

Research

keywords

  • Cell Movement
  • Cell Surface Extensions
  • Membrane Glycoproteins
  • Microfilament Proteins

Identity

PubMed Central ID

  • PMC7511357

Scopus Document Identifier

  • 85091463577

Digital Object Identifier (DOI)

  • 10.1109/TSMC.1979.4310076

PubMed ID

  • 32968060

Additional Document Info

volume

  • 11

issue

  • 1