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Article
Nature Immunology  1, 342 - 347 (2000)
doi:10.1038/79801

Role of Drosophila IKKbig gamma in a Toll-independent antibacterial immune response

Sophie Rutschmann1, Alain C. Jung1, Rui Zhou2, Neal Silverman2, Jules A. Hoffmann1 & Dominique Ferrandon1

1  Institut de Biologie Moléculaire et Cellulaire, UPR 9022 du CNRS, 15, rue R. Descartes, F67084 Strasbourg Cedex, France.

2  Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.

Correspondence should be addressed to Dominique Ferrandon d.ferrandon@ibmc.u-strasbg.fr
We have generated, by ethylmethane sulfonate mutagenesis, loss-of-function mutants in the Drosophila homolog of the mammalian I-kappaB kinase (IKK) complex component IKKbold gamma (also called NEMO). Our data show that Drosophila IKKbold gamma is required for the Relish-dependent immune induction of the genes encoding antibacterial peptides and for resistance to infections by Escherichia coli. However, it is not required for the Toll-DIF−dependent antifungal host defense. The results indicate distinct control mechanisms of the Rel-like transactivators DIF and Relish in the Drosophila innate immune response and show that Drosophila Toll does not signal through a IKKbold gamma-dependent signaling complex. Thus, in contrast to the vertebrate inflammatory response, IKKbold gamma is required for the activation of only one immune signaling pathway in Drosophila.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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