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First published online 2 August 2005
doi: 10.1242/jcs.02491

Journal of Cell Science 118, 3717-3726 (2005)
Published by The Company of Biologists 2005
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Research Article

Abl tyrosine kinase regulates a Rac/JNK and a Rac/Nox pathway for DNA synthesis and Myc expression induced by growth factors

Anthony Boureux, Olivia Furstoss*, Valérie Simon and Serge Roche{ddagger}

CRBM, CNRS FRE2593, 1919 route de Mende, 34293 Montpellier Cedex 05, France

{ddagger} Author for correspondence (e-mail: serge.roche{at}crbm.cnrs.fr)

Accepted 13 May 2005

The cytoplasmic tyrosine kinase Abl is a Src substrate required for platelet-derived growth factor (PDGF) receptor signaling leading to Myc expression and DNA synthesis. Abl targets are, however, ill defined. Here we report that the small GTPase Rac is an important effector of its mitogenic function. PDGF-induced Rac activation was impaired in cells with inactive Abl and active Rac overcame the mitogenic defects found in these cells. Rac function required both a Jun N-terminal kinase (JNK) and a NADPH oxidase (Nox) pathway. Furthermore, co-activation of JNK and Nox were sufficient to mimic the Rac mitogenic rescue. Abl also regulated PDGF-induced JNK and Nox activation. Finally, we found that Myc is an important target of this signaling cascade: Myc induction was sensitive to small inhibitors of JNK and Nox activities and forced expression of Myc overcame the G1 block induced by dominant interfering mutants of mitogen-activated protein kinase kinase 4 (MKK4) and Nox2 activating subunit. We concluded that cytoplasmic Abl operates on a Rac/JNK and a Rac/Nox pathway for PDGF-induced Myc induction and DNA synthesis.

Key words: Src, Abl, PDGF Receptor, Rac, Mitogenesis, Signaling


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© The Company of Biologists Ltd 2005