Journal
JOURNAL OF CELL SCIENCE
Volume 121, Issue 12, Pages 1981-1989Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.025130
Keywords
spreading; migration; fibronectin; ELMO; Dock180
Categories
Funding
- NIGMS NIH HHS [R01 GM 47214, R01 GM047214, R01 GM047214-19] Funding Source: Medline
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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.
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