Mitochondrial ATP-sensitive potassium channel activity and hypoxic preconditioning are independent of an inwardly rectifying potassium channel subunit in C. elegans

Hypoxic preconditioning (HP) is an evolutionarily-conserved mechanism that protects an organism against stress. The mitochondrial ATP-sensitive K + channel (mK ATP ) plays an essential role in the protective signaling, but remains molecularly undefined. Several lines of evidence suggest that mK ATP may arise from an inward rectifying K + channel (Kir). The genetic model organism C. elegans exhibits HP and displays mK ATP activity. Here, we investigate the tissue expression profile of the three C. elegans Kir genes and demonstrate that mutant strains where the irk genes have been deleted either individually or in combination can be protected by HP and exhibit robust mK ATP channel activity in purified mitochondria. These data suggest that the mK ATP in C. elegans does not arise from a Kir derived channel.