| First Author | Haynes EM | Year | 2015 |
| Journal | J Cell Biol | Volume | 209 |
| Issue | 6 | Pages | 803-12 |
| PubMed ID | 26101216 | Mgi Jnum | J:227313 |
| Mgi Id | MGI:5700142 | Doi | 10.1083/jcb.201501094 |
| Citation | Haynes EM, et al. (2015) GMFbeta controls branched actin content and lamellipodial retraction in fibroblasts. J Cell Biol 209(6):803-12 |
| abstractText | 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 GMFbeta, 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 that depletion of GMFbeta 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 GMFbeta in vivo. Furthermore, depletion or overexpression of GMFbeta disrupted the ability of cells to directionally migrate to a gradient of fibronectin (haptotaxis). These data suggest that debranching by GMFbeta plays an important role in branched actin regulation, lamellipodial dynamics, and directional migration. |
