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Prepublished online as a Blood First Edition Paper on July 12, 2002; DOI 10.1182/blood-2002-01-0154.
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Blood, 1 November 2002, Vol. 100, No. 9, pp. 3183-3192
HEMATOPOIESIS
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
From The Biomedical Research Centre, University of
British Columbia, Vancouver, British Columbia, Canada.
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), and 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 about 25% to 30% of Rac-1 activation
still occurring in the absence of detectable increases in
phosphatidyl-inositol-3 kinase (PI-3K) activity. Overexpression of
constitutively active mutants of H-Ras, N-Ras, or M-Ras resulted in
activation of coexpressed Rac-1 through an Ly29402-resistant, PI-3K-independent mechanism.
Overexpression of constitutively active mutants of p21 Ras, or Rac-1,
but not of PI-3K, was sufficient for activation of p38
mitogen-activated protein kinase (MAPK) in cells of hemopoietic origin.
Inhibition of increases in PI-3K activity by Ly294002 had no effect on
the IL-3-induced activation of p38 MAPK. In contrast, Ly294002
partially inhibited the activation of p38 MAPK induced by
cross-linking of the BCR, although some p38 MAPK activation occurred in
the absence of increases in the activity of Rac-1 or PI-3K. 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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