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A more recent version of this article appeared on May 1, 2006
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Submitted on October 14, 2005
Revised on January 30, 2006
Accepted on February 27, 2006
*Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115; Department of Genetics, Children’s Hospital Boston, Boston, MA 02115
Monitoring Editor: Mark Ginsberg
Previous studies of Rac1 in fibroblasts have used dominant negative constructs, which may have nonspecific effects. We used a conditional Rac1 allele to critically examine Rac1 function in mouse fibroblasts. Lack of Rac1 had dramatic effects on nonconfluent cells, which were elongated and had extensive blebbing, but no lamellipodia or ruffle formation. However, Rac1 null fibroblasts translocated using pseudopodia-like protrusions without lamellipodia, migrating toward a PDGF gradient as efficiently as their wild type counterparts. Rac1 null fibroblasts closed wounds in vitro and spread on a fibronectin substrate, although at a slower rate than wild type cells. However, Rac1 null cells were markedly impaired in proliferation, with a defect in G1 to S transition, although they were capable of surviving in culture for over 2 wk. These results refine our understanding of the functions of Rac1, indicate that lamellipodia formation is not required for cell motility, and show that PDGF-induced chemotaxis can occur in the absence of both lamellipodia and Rac1.
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