Role of Drosophila IKKγ in a Toll-independent antibacterial immune response

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Abstract
We have generated, by ethylmethane sulfonate mutagenesis, loss-of-function mutants in the Drosophila homolog of the mammalian I-κB kinase (IKK) complex component IKKγ (also called NEMO). Our data show that Drosophila IKKγ 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 IKKγ-dependent signaling complex. Thus, in contrast to the vertebrate inflammatory response, IKKγ is required for the activation of only one immune signaling pathway in Drosophila.