We have generated, by ethylmethane sulfonate mutagenesis, loss-of-function
mutants in the Drosophila homolog of the mammalian I-kappa B kinase (IKK) c
omplex component IKK gamma (also called NEMO). Our data show that Drosophil
a IKK gamma is required for the Relish-dependent immune induction of the ge
nes encoding antibacterial peptides and for resistance to infections by Esc
herichia coli. However, it is not required for the Toll-Dip-dependent antif
ungal host: defense,The results indicate distinct control mechanisms of the
Rel-like transactivators DIF and Relish in the Drosophila innate immune re
sponse and show that Drosophila Toll does not signal through a IKK gamma-de
pendent signaling complex. Thus, in contrast to the vertebrate inflammatory
response, IKK gamma is required for the activation of only one immune sign
aling pathway in Drosophila.