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J. Biol. Chem., Vol. 278, Issue 49, 48928-48934, December 5, 2003

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Immune Activation of NF-B and JNK Requires Drosophila TAK1^*

Neal Silverman¶, Rui Zhou, Rachel L. Erlich||**, Mike Hunter, Erik Bernstein, David Schneider, and Tom Maniatis

From the Division of Infectious Disease, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, the Department of Molecular and Cellular Biology and the ^||Bauer Center for Genomic Research, Harvard University, Cambridge, Massachusetts 02138, the Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02139, and the Department of Microbiology and Immunology, Stanford Medical School, Stanford, California 94305

Stimulation of the Drosophila immune response activates NF-B and JNK signaling pathways. For example, infection by Gram-negative bacteria induces the Imd signaling pathway, leading to the activation of the NF-B-like transcription factor Relish and the expression of a battery of genes encoding antimicrobial peptides. Bacterial infection also activates the JNK pathway, but the role of this pathway in the immune response has not yet been established. Genetic experiments suggest that the Drosophila homolog of the mammalian MAPK kinase kinase, TAK1 (transforming growth factor -activated kinase 1), activates both the JNK and NF-B pathways following immune stimulation. In this report, we demonstrate that Drosophila TAK1 functions as both the Drosophila IB kinase-activating kinase and the JNK kinase-activating kinase. However, we found that JNK signaling is not required for antimicrobial peptide gene expression but is required for the activation of other immune inducible genes, including Punch, sulfated, and malvolio. Thus, JNK signaling appears to play an important role in the cellular immune response and the stress response.

Received for publication, May 7, 2003 , and in revised form, September 16, 2003.

^* This work was supported by National Institutes of Health Grants GM59919 and GM29379 (to T. M.). 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.

The on-line version of this article (available at http://www.jbc.org) contains Supplemental Fig. 1.

^** Present address: Dept. of Biology, Massachusetts Inst. of Technology, Cambridge, MA 01239.

^¶ To whom correspondence should be addressed: 364 Plantation Rd., LRB 313, Worcester, MA 01605. Tel.: 508-856-5826; Fax: 508-856-5463; E-mail: neal.silverman{at}umassmed.edu.

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