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Prepublished online as a Blood First Edition Paper on July 12, 2002; DOI 10.1182/blood-2002-01-0154.
Submitted January 17, 2002
Accepted June 10, 2002
Activation of Rac-1, Rac-2 and Cdc42 by hemopoietic growth factors or cross-linking of the B lymphocyte receptor for antigen
Brock Grill and John W Schrader*
The Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada
* Corresponding author; email: john{at}brc.ubc.ca.
Interleukin-3 (IL-3) induced activation of endogenous Rac-1, Rac-2 and Cdc42. Rac-1 was also activated by colony-stimulating factor-1 (CSF-1), Steel locus factor (SLF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-5 (IL-5), or by cross-linking the B lymphocyte receptor for antigen (BCR). The activation of Rac-1 induced by cross-linking the BCR or by IL-3 stimulation was blocked only partially by Ly294002, with ~ 25-30% of Rac-1 activation still occurring in the absence of detectable increases in PI-3K activity. Over-expression of constitutively active mutants of H-Ras, N-Ras or M-Ras resulted in activation of co-expressed Rac-1 through an Ly294002-resistant, PI-3K-independent mechanism. Over-expression of constitutively active mutants of p21 Ras, or Rac-1, but not of PI-3K, was sufficient for activation of p38 MAPK in cells of hemopoietic origin. However, Ly294002 had no effect on the IL-3 induced activation of p38 MAPK. In contrast, while Ly294002 inhibited a fraction of the activation of p38 MAPK induced by cross-linking of the BCR, in parallel with inhibition of the activity of PI-3K and Rac-1, another fraction of p38 MAPK activation occurred in the absence of increases in Rac-1 or PI-3K activity. The activation of Rac-1, Rac-2, and Cdc42 by IL-3 and other hemopoietic growth factors is likely to be an important component of their actions in promoting growth, survival and function.
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