GMFβ Controls Branched Actin Content and Lamellipodial Retraction in Fibroblasts Public Deposited

Downloadable Content

Download PDF
Last Modified
  • March 22, 2019
Creator
  • Haynes, Elizabeth
    • Affiliation: School of Medicine, Department of Cell Biology and Physiology
Abstract
  • The lamellipodium is an important structure for cell migration containing branched actin nucleated via the Arp2/3 complex. The formation of branched actin is relatively well studied, but less is known about its disassembly and how this influences migration. GMF is implicated in both Arp2/3 debranching and inhibition of Arp2/3 activation. Modulation of GMFβ, a ubiquitous GMF isoform, by depletion or overexpression resulted in changes in lamellipodial dynamics, branched actin content and migration. Acute pharmacological inhibition of Arp2/3 by CK-666, coupled to quantitative live-cell imaging of the complex, showed depletion of GMFβ decreased the rate of branched actin disassembly. These data, along with mutagenesis studies, suggest that debranching (not inhibition of Arp2/3 activation) is a primary activity of GMFβ in vivo. Furthermore, depletion or overexpression of GMFβ disrupted the ability of cells to directionally migrate to a gradient of fibronectin (haptotaxis). These data suggest that debranching by GMFβ plays an important role in branched actin regulation, lamellipodial dynamics, and directional migration.
Date of publication
Keyword
Subject
Identifier
Resource type
Rights statement
  • In Copyright
Advisor
  • Rogers, Stephen
  • Gupton, Stephanie
  • Bear, James
  • Cheney, Richard
  • Mack, Christopher P.
Degree
  • Doctor of Philosophy
Degree granting institution
  • University of North Carolina at Chapel Hill Graduate School
Graduation year
  • 2015
Language
Publisher
Place of publication
  • Chapel Hill, NC
Access
  • There are no restrictions to this item.
Parents:

This work has no parents.

Items