Meeting Abstract
The annual killifish Austrofundulus limnaeus inhabits ephemeral ponds in the Maracaibo Basin of Venezuela. Permanent populations of A. limnaeus are maintained only by the production of stress-tolerant embryos that can enter a state of metabolic dormancy and developmental arrest, termed diapause. A. limnaeus embryos are able to tolerate longer periods of anoxia than any other vertebrate yet studied. Because insufficient oxygen supply to mitochondria has long been known to cause electron transport chain dysfunction, the ability of A. limnaeus embryonic mitochondria to tolerate such long periods of anoxia is of great interest. Previous work has suggested that in anoxia- and hypoxia-sensitive mammalian models, exposure of cells to low oxygen conditions can result in mitochondrial autophagy (mitophagy) or mitochondrial biogenesis following reoxygenation. Here, we measure changes in relative mtDNA copy number following anoxia/reoxygenation in A. limnaeus embryos to give an indication of mitochondrial degradation and biogenesis during normoxic and anoxic conditions. We also describe the first complete mitochondrial genome sequence of A. limnaeus and compare its sequence and synteny to other species within the Order Cyprinodontiformes. Interestingly, we did not observe changes in relative mtDNA content following anoxia/reoxygenation treatment in A. limnaeus embryos, suggesting that mitophagy or mitochondrial biogenesis may not have a role in A. limnaeus anoxia tolerance. However, we did find mtgenome sequence rearrangements that are unique to A. limnaeus when compared to other fish species. These results suggest that mtDNA copy number stability may be important for tolerating periods of anoxia, and also indicate that there may be unique mtDNA sequence that can facilitate extreme anoxia tolerance.
