| First Author | Meller J | Year | 2008 |
| Journal | J Cell Sci | Volume | 121 |
| Issue | Pt 12 | Pages | 1981-9 |
| PubMed ID | 18505794 | Mgi Jnum | J:139771 |
| Mgi Id | MGI:3810034 | Doi | 10.1242/jcs.025130 |
| Citation | Meller J, et al. (2008) Endogenous RhoG is dispensable for integrin-mediated cell spreading but contributes to Rac-independent migration. J Cell Sci 121(Pt 12):1981-9 |
| abstractText | Rac activation by integrins is essential for cell spreading, migration, growth and survival. Based mainly on overexpression of dominant-negative mutants, RhoG has been proposed to mediate integrin-dependent Rac activation upstream of ELMO and Dock180. RhoG-knockout mice, however, display no significant developmental or functional abnormalities. To clarify the role of RhoG in integrin-mediated signaling, we developed a RhoG-specific antibody, which, together with shRNA-mediated knockdown, allowed analysis of the endogenous protein. Despite dramatic effects of dominant-negative constructs, nearly complete RhoG depletion did not substantially inhibit cell adhesion, spreading, migration or Rac activation. Additionally, RhoG was not detectably activated by adhesion to fibronectin. Using Rac1(-/-) cells, we found that constitutively active RhoG induced membrane ruffling via both Rac-dependent and -independent pathways. Additionally, endogenous RhoG was important for Rac-independent cell migration. However, RhoG did not significantly contribute to cell spreading even in these cells. These data therefore clarify the role of RhoG in integrin signaling and cell motility. |
