Cooperative control of Drosophila immune responses by the JNK and NF-κB signaling pathways

被引:146
作者
Delaney, Joseph R.
Stoven, Svenja
Uvell, Hanna
Anderson, Kathryn V.
Engstrom, Ylva
Mlodzik, Marek
机构
[1] Mt Sinai Sch Med, Brookdale Dept Dev Cell & Mol Biol, New York, NY 10029 USA
[2] Mt Sinai Sch Med, Dept Oncol Sci, New York, NY 10029 USA
[3] Umea Univ, Ctr Mol Pathogenesis, Umea, Sweden
[4] Stockholm Univ, Dept Mol Biol & Funct Genom, Stockholm, Sweden
[5] Mem Sloan Kettering Canc Ctr, Dev Biol Program, Sloan Kettering Inst, New York, NY 10021 USA
关键词
Drosophila; innate immunity; JNK; NF-kappa B; relish;
D O I
10.1038/sj.emboj.7601182
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3068 / 3077
页数:10
相关论文
共 65 条
[1]   Distortion of proximodistal information causes JNK-dependent apoptosis in Drosophila wing [J].
Adachi-Yamada, T ;
Fujimura-Kamada, K ;
Nishida, Y ;
Matsumoto, K .
NATURE, 1999, 400 (6740) :166-169
[2]   Signaling role of hemocytes in Drosophila JAK/STAT-dependent response to septic injury [J].
Agaisse, H ;
Petersen, UM ;
Boutros, M ;
Mathey-Prevot, B ;
Perrimon, N .
DEVELOPMENTAL CELL, 2003, 5 (03) :441-450
[3]  
Behrens J, 2000, J CELL SCI, V113, P911
[4]   DROSOPHILA JUN MEDIATES RAS-DEPENDENT PHOTORECEPTOR DETERMINATION [J].
BOHMANN, D ;
ELLIS, MC ;
STASZEWSKI, LM ;
MLODZIK, M .
CELL, 1994, 78 (06) :973-986
[5]   Sequential activation of signaling pathways during innate immune responses in Drosophila [J].
Boutros, M ;
Agaisse, H ;
Perrimon, N .
DEVELOPMENTAL CELL, 2002, 3 (05) :711-722
[6]  
BRAND AH, 1993, DEVELOPMENT, V118, P401
[7]   Drosophila:: The genetics of innate immune recognition and response [J].
Brennan, CA ;
Anderson, KV .
ANNUAL REVIEW OF IMMUNOLOGY, 2004, 22 :457-483
[8]   Discrete functions of TRAF1 and TRAF2 in Drosophila melanogaster mediated by c-Jun N-terminal kinase and NF-κB-dependent signaling pathways [J].
Cha, GH ;
Cho, KS ;
Lee, JH ;
Kim, M ;
Kim, E ;
Park, J ;
Lee, SB ;
Chung, J .
MOLECULAR AND CELLULAR BIOLOGY, 2003, 23 (22) :7982-7991
[9]   mom identifies a receptor for the Drosophila JAK/STAT signal transduction pathway and encodes a protein distantly related to the mammalian cytokine receptor family [J].
Chen, HW ;
Chen, X ;
Oh, SW ;
Marinissen, MJ ;
Gutkins, JS ;
Hou, SX .
GENES & DEVELOPMENT, 2002, 16 (03) :388-398
[10]   Toll-like receptors and T-helper-1/T-helper-2 responses [J].
Dabbagh, K ;
Lewis, DB .
CURRENT OPINION IN INFECTIOUS DISEASES, 2003, 16 (03) :199-204