[Abstract]  [Full Text]  [PDF]

David Bond¹, David A. Primrose¹ and Edan Foley^1*

¹ Department of Medical Microbiology and Immunology, University of Alberta. Edmonton AB. Canada.

* To whom correspondence should be addressed: Edan Foley, Department of Medical Microbiology and Immunology, University of Alberta. Edmonton AB. Canada. Phone: (780) 492-2303. Fax: (780) 492-9828. Email: efoley@ualberta.ca

Biol. Proced. Online 2008;10:20-28. doi:10.1251/bpo139
Submitted: September 24, 2007; Accepted: December 09, 2007; Published: February 04, 2008.

Indexing terms: RNA interference; immunity; drosophila.

Abbreviations: IKK, I-kappa kinase; Imd, immune deficiency; JNK, c-Jun N-terminal kinase; PGN, gram-negative bacterial peptidoglycan; PGRP-LC, peptidoglycan recognition protein-LC; TNF, tumor necrosis factor.

Drosophila activates a robust defense response to gram-negative bacteria through the Immune deficiency (Imd) pathway. Imd signaling proceeds through c-Jun N-terminal Kinase (JNK), NF-kB and caspase modules. The individual signaling modules act in a highly coordinated manner to yield a stereotypical response to infection. While considerable attention has focused on NF-kB-mediated antimicrobial activities, more recent studies have highlighted the involvement of JNK signaling in the Imd pathway response. JNK signaling occurs in a transitory burst and drives the expression of a number of gene products through the AP-1 transcription factor. In this report, we describe a simple method for the quantification of JNK activation by Western blot analysis or directly in tissue culture plates.