Hypoxia activates IKK-NF-κB and the immune response in Drosophila melanogaster

Biosci Rep. 2014 Jul 29;34(4):e00127. doi: 10.1042/BSR20140095.

Abstract

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-κB (nuclear factor κB). Here we show that hypoxia activates the IKK-NF-κB [IκB (inhibitor of nuclear factor κB)-NF-κB] pathway and the immune response in Drosophila melanogaster. We show that NF-κB activation is required for organism survival in hypoxia. Finally, we identify a role for the tumour suppressor Cyld, as a negative regulator of NF-κB in response to hypoxia in Drosophila. The results indicate that hypoxia activation of the IKK-NF-κB pathway and the immune response is an important and evolutionary conserved response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Deubiquitinating Enzyme CYLD
  • Drosophila Proteins / genetics
  • Drosophila melanogaster / genetics*
  • Drosophila melanogaster / immunology*
  • HeLa Cells
  • Humans
  • Hypoxia / genetics*
  • I-kappa B Proteins / genetics*
  • NF-kappa B / genetics*
  • Signal Transduction / genetics
  • Signal Transduction / immunology
  • Tumor Suppressor Proteins / genetics

Substances

  • Drosophila Proteins
  • I-kappa B Proteins
  • NF-kappa B
  • Tumor Suppressor Proteins
  • CYLD protein, Drosophila
  • Deubiquitinating Enzyme CYLD