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