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J. Biol. Chem., Vol. 282, Issue 44, 32121-32127, November 2, 2007

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Stress-induced c-Jun Activation Mediated by Polo-like Kinase 3 in Corneal Epithelial Cells^*

Ling Wang, Wei Dai, and Luo Lu¹

From the Department of Medicine, Harbor-UCLA Medical Center, David Geffen School of Medicine, University of California Los Angeles, Torrance, California 90502 and the Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987

Polo-like kinase 3 (Plk3) activation occurs after exposure to environmental or genotoxic stresses. Plk3 regulates cell fate through regulating cell cycle progression. UV irradiation is one of the major environmental stresses that affect corneal epithelial wound healing. In the present study, we report that UV irradiation activated Plk3 and that Plk3 interacts with AP-1 and c-Jun, which appears to be important to mediate corneal epithelial cell apoptosis after UV irradiation. Recombinant Plk3, as well as Plk3 immunoprecipitated from UV-irradiated cells, phosphorylated c-Jun in vitro. The phosphorylation of c-Jun by Plk3 immunoprecipitates was not altered by the pre-removal of JNK from the cell lysates. In addition, the effect of UV irradiation-induced phosphorylation of c-Jun and apoptosis were not significantly affected by knockdown of JNK mRNA. Co-immunoprecipitation reveals that Plk3 and c-Jun directly interacted with each other. Consistently, Plk3 co-localized with c-Jun to the nucleus after UV irradiation. Further, modulating Plk3 activities by overexpressing Plk3 or its mutants significantly affected UV irradiation-induced c-Jun activity and subsequent apoptosis. Our results thus provide for the first time that Plk3 mediates UV irradiation-induced c-Jun activation by phosphorylating c-Jun, suggesting that Plk3 plays an important role in mediating programmed cell death of corneal epithelial cells after UV irradiation.

Received for publication, April 2, 2007 , and in revised form, August 15, 2007.

^* This work was supported by National Institutes of Health Grants EY12953 (to L. L.) and CA074229 (to W. D.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: Dept. of Medicine, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA, 1124 W. Carson St., C-2, Torrance, CA 90502. Tel.: 310-787-6853; Fax: 310-222-3781; E-mail: lluou{at}ucla.edu.

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