Hypoxia, or low oxygen availability, is an important physiological and
pathological stimulus for multicellular organisms. Molecularly, hypoxia
activates a transcriptional programme directed at restoration of oxygen
homoeostasis and cellular survival. In mammalian cells, hypoxia not only
activates the HIF (hypoxia-inducible factor) family, but also
additional transcription factors such as NF-?B (nuclear factor ?B). Here
we show that hypoxia activates the IKK–NF-?B [I?B (inhibitor of nuclear
factor ?B)–NF-?B] pathway and the immune response in Drosophila melanogaster.
We show that NF-?B activation is required for organism survival in
hypoxia. Finally, we identify a role for the tumour suppressor Cyld, as a
negative regulator of NF-?B in response to hypoxia in Drosophila.
The results indicate that hypoxia activation of the IKK–NF-?B pathway
and the immune response is an important and evolutionary conserved