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Cooperative control of Drosophila immune responses by the JNK and NF‐κB signaling pathways
Author(s) -
Delaney Joseph R,
Stöven Svenja,
Uvell Hanna,
Anderson Kathryn V,
Engström Ylva,
Mlodzik Marek
Publication year - 2006
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601182
Subject(s) - biology , signal transduction , immune system , nf κb , microbiology and biotechnology , nfkb1 , drosophila (subgenus) , phosphorylation , genetics , transcription factor , gene
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‐κB/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.