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Originally published In Press as doi:10.1074/jbc.M205485200 on October 10, 2002

J. Biol. Chem., Vol. 277, Issue 50, 48372-48378, December 13, 2002
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Activation of SAPK/JNK Signaling by Protein Kinase Cdelta in Response to DNA Damage*

Kiyotsugu YoshidaDagger , Yoshio MikiDagger , and Donald Kufe§

From the  Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115 and Dagger  Department of Molecular Genetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan

The cellular response to genotoxic stress includes activation of protein kinase Cdelta (PKCdelta ). The functional role of PKCdelta in the DNA damage response is unknown. The present studies demonstrate that PKCdelta is required in part for induction of the stress-activated protein kinase (SAPK/JNK) in cells treated with 1-beta -D-arabinofuranosylcytosine (araC) and other genotoxic agents. DNA damage-induced SAPK activation was attenuated by (i) treatment with rottlerin, (ii) expression of a kinase-inactive PKCdelta (K-R) mutant, and (iii) down-regulation of PKCdelta by small interfering RNA (siRNA). Coexpression studies demonstrate that PKCdelta activates SAPK by an MKK7-dependent, SEK1-independent mechanism. Previous work has shown that the nuclear Lyn tyrosine kinase activates the MEKK1 right-arrow MKK7 right-arrow SAPK pathway but not through a direct interaction with MEKK1. The present results extend those observations by demonstrating that Lyn activates PKCdelta , and in turn, MEKK1 is activated by a PKCdelta -dependent mechanism. These findings indicate that PKCdelta functions in the activation of SAPK through a Lyn right-arrow PKCdelta right-arrow MEKK1 right-arrow MKK7 right-arrow SAPK signaling cascade in response to DNA damage.

* This work was supported by NCI, National Institutes of Health Grants CA29431 and CA55241.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed. Tel.: 617-632-3141; Fax: 617-632-2934; E-mail: Donald-Kufe@dfci.harvard.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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