Genetics, Vol. 159, 189-199, September 2001, Copyright © 2001

Drosophila Immunity: Genes on the Third Chromosome Required for the Response to Bacterial Infection

Louisa P. Wua,b, Kwang-Min Choeb,c, Yiran Lub,c, and Kathryn V. Andersonb
a Center for Agricultural Biotechnology, University of Maryland Biotechnology Institute, College Park, Maryland 20742,
b Molecular Biology Program, Sloan-Kettering Institute, New York, New York 10021
c Molecular and Cell Biology Program, Cornell University, Weill Graduate School of Medical Sciences, New York, New York 10021

Corresponding author: Kathryn V. Anderson, Sloan-Kettering Institute, 1275 York Ave., New York, NY 10012., k-anderson{at}ski.mskcc.org (E-mail)

Communicating editor: T. SCHÜPBACH

We have screened the third chromosome of Drosophila melanogaster for mutations that prevent the normal immune response. We identified mutant lines on the basis of their failure to induce transcription of an antibacterial peptide gene in response to infection or their failure to form melanized clots at the site of wounding. These mutations define 14 genes [immune response deficient (ird) genes] that have distinct roles in the immune response. We have identified the molecular basis of several ird phenotypes. Two genes, scribble and kurtz/modulo, affect the cellular organization of the fat body, the tissue responsible for antimicrobial peptide production. Two ird genes encode components of the signaling pathways that mediate responses to bacterial infection, a Drosophila gene encoding a homolog of I{kappa}B kinase (DmIkkß) and Relish, a Rel-family transcription factor. These genetic studies should provide a basis for a comprehensive understanding of the genetic control of immune responses in Drosophila.




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