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Originally published In Press as doi:10.1074/jbc.M207391200 on October 24, 2002

J. Biol. Chem., Vol. 278, Issue 1, 567-572, January 3, 2003
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A Single c-Jun N-terminal Kinase Isoform (JNK3-p54) Is an Effector in Both Neuronal Differentiation and Cell Death*

Vicki Waetzig and Thomas HerdegenDagger

From the Institute of Pharmacology, Kiel University Medical Center, D-24105 Kiel, Germany

The c-Jun N-terminal kinases (JNKs) mediate degeneration and apoptosis in the brain. Particularly, JNK3 is considered to be a degenerative enzyme with c-Jun as a relevant substrate. The contribution of individual JNK isoforms, however, to pathological as well as to physiological processes remains to be defined. To analyze the effects of a single JNK isoform on neuronal cell death and differentiation, we transfected PC12 cells, which normally express only JNK1 and JNK2, with JNK3-p54. Transfected JNK3 significantly enhanced cell death after UV irradiation (0.5-6 J/cm2) and paclitaxel/taxol treatment (1-10 µM). In contrast, in the context of nerve growth factor-induced (10 or 50 ng/ml) differentiation of PC12 cells, JNK3 expression significantly increased the number and length of neurites. This functional dichotomy of JNK3 was mirrored by differential activation and induction of nuclear JNK substrates; although activating transcription factor-2 phosphorylation was enhanced by death signaling in response to UV and taxol, c-Jun protein expression and N-terminal phosphorylation were increased during nerve growth factor-induced differentiation. The absence of significant JNK activation or target phosphorylation in response to H2O2 (60 µM) further supports the hypothesis that JNK isoforms are not merely injury- or stress-specific kinases but also have context-specific physiological functions.

* This work was supported by the Deutsche Forschungsgemeinschaft.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.

Dagger To whom correspondence should be addressed: Inst. of Pharmacology, Kiel University Medical Center, Hospitalstrasse 4, D-24105 Kiel, Germany. Tel.: 49-431-597-3502; Fax: 49-431-597-3522, E-mail: t.herdegen@pharmakologie.uni-kiel.de.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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