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Meeting Abstract
The anoxia-tolerant turtle, Trachemys scripta is able to survive months buried in anoxic mud while overwintering in ice covered-ponds. In most vertebrates, anoxia leads to inner mitochondrial membrane depolarization causing the F1FO-ATPase to run in reverse, hydrolyzing ATP, in an effort to restore membrane potential. This depolarization triggers a signalling cascade ending in cellular apoptosis or necrosis. Previous studies have shown that when T. scripta is exposed to anoxia, they severely down-regulate F1FO-ATPase activity. The benefits of reducing F1FO-ATPase activity during anoxia are clear, but the mechanisms responsible for inhibition remain unknown. Inhibitory Factor-1, a well-characterized mitochondrial ATPase inhibitor, is not responsible for the inhibition of F1FO-ATPase in T. scripta. We predict that during long-term anoxia, the F1FO-ATPase is inhibited via post-transnational modification, which we investigated using proteomics approaches.