Journal
EMBO JOURNAL
Volume 25, Issue 13, Pages 3068-3077Publisher
WILEY
DOI: 10.1038/sj.emboj.7601182
Keywords
Drosophila; innate immunity; JNK; NF-kappa B; relish
Categories
Funding
- NCI NIH HHS [T32-CA86796] Funding Source: Medline
- NEI NIH HHS [R01 EY013256, R01-EY13256] Funding Source: Medline
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Jun N-terminal kinase (JNK) signaling is a highly conserved pathway that controls both cytoskeletal remodeling and transcriptional regulation in response to a wide variety of signals. Despite the importance of JNK in the mammalian immune response, and various suggestions of its importance in Drosophila immunity, the actual contribution of JNK signaling in the Drosophila immune response has been unclear. Drosophila TAK1 has been implicated in the NF-kappa B/Relish-mediated activation of antimicrobial peptide genes. However, we demonstrate that Relish activation is intact in dTAK1 mutant animals, and that the immune response in these mutant animals was rescued by overexpression of a downstream JNKK. The expression of a JNK inhibitor and induction of JNK loss-of-function clones in immune responsive tissue revealed a general requirement for JNK signaling in the expression of antimicrobial peptides. Our data indicate that dTAK1 is not required for Relish activation, but instead is required in JNK signaling for antimicrobial peptide gene expression.
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