|
 |
|
|
| Subject Categories: Signal Transduction | Immunology |
|
| The EMBO Journal
(2006) 25, 3068–3077, doi:10.1038/sj.emboj.7601182 Published online 8 June 2006 |
|
Cooperative control of Drosophila immune responses by the JNK and NF- B signaling pathways |
|
|
| Joseph R Delaney1, Svenja Stöven2, Hanna Uvell3, Kathryn V Anderson4, Ylva Engström3 and Marek Mlodzik1 |
|
|
1 Brookdale Department of Developmental, Cell and Molecular Biology and Department of Oncological Sciences, The Mount Sinai School of Medicine, New York, NY, USA 2 Umeå Center for Molecular Pathogenesis, Umeå University, Umeå, Sweden 3 Department of Molecular Biology and Functional Genomics, Stockholm University, Stockholm, Sweden 4 Developmental Biology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY, USA To whom correspondence should be addressed Marek Mlodzik, The Mount Sinai School of Medicine, One Gustave L Levy Place, Box 1020, New York, NY 10029, USA. Tel.: +1 212 241 6516; Fax: +1 212 241 8610; E-mail: marek.mlodzik@mssm.edu Received 21 October 2005; Accepted 15 May 2006; Published online 8 June 2006. |
|
|
|
| Abstract |
|
| 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-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. |
|
| Keywords:
Drosophila
, innate immunity, JNK, NF-B, Relish |
|
|
|
Top of page MORE ARTICLES LIKE THISThese links to content published by NPG are automatically generated NEWS AND VIEWSNature's fortress against infection Nature Immunology News and Views (01 May 2004) Nature Immunology News and Views (01 Jan 2008) RESEARCHThe Toll and Imd pathways are the major regulators of the immune response in Drosophila The EMBO Journal Article (03 Jun 2002) Inhibitor of apoptosis 2 and TAK1-binding protein are components of the Drosophila Imd pathway The EMBO Journal Article (05 Oct 2005) |
|
|
| |
| |
| |
 | Email link to a friend |
| |
 | Download PDF |
| |
 | Full text |
| |
| |
| |
 | Next article |
| |
 | Previous article |
| |
 | Table of contents |
| |
| |
 | Rights and permissions |
| |
 | Reprints |
| |
| |
| |
 Register for table of contents by email | |
| |
| |
| |