Meeting Abstract
P2.15 Saturday, Jan. 5 Expression levels of cell cycle regulator Akt (PKB) reveals contradictory results during diapause and anoxia-induced dormancy in embryos of the annual killifish Austrofundulus limnaeus. CULPEPPER, K.M.*; PODRABSKY, J.E.; Portland State University; Portland State University kristin8@pdx.edu
Understanding the molecular underpinnings of anoxia tolerance may aid in the prevention and treatment of stroke and ischemia in humans. Embryos of the annual killifish, Austrofundulus limnaeus, enter a state of metabolic and developmental arrest termed diapause II (DII) in order to survive the dry season of their natural habitats, ephemeral ponds in South America. Additionally, previous reports show that throughout development A. limnaeus embryos have 2-fold magnitude higher anoxia tolerance than any other vertebrate studied, making them an excellent model to study the effects of oxygen deprivation. Due to this astonishing feat, we examined the role of Akt (Protein Kinase B), a serine/threonine-specific kinase involved with G1– to S-phase transitions, across development of A. limnaeus embryos and in response to anoxia. Immunoblot results revealed that phosphorylated Akt (pAkt) levels steadily increased following fertilization, peaked at DII, and decreased during subsequent development, except for a stage-specific spike in concentration at 12 days post-DII (dpd). These data suggest that cell cycle arrest associated with entrance into DII is not regulated by low levels of pAKT. Next, we assayed pAkt levels in 12 dpd embryos subjected to 1h and 48h of anoxia, followed by 1h, 6h, and 24h of recovery. Levels of pAkt were significantly reduced following 48h exposure to anoxia and protein expression returned to control levels by 6h of normoxia. This suggests that pAkt may play a role in arresting cell cycle progression in embryos exposed to prolonged anoxia. Overall, our results indicate a contradictory role for pAkt in cell cycle regulation associated with diapause and anoxia-induced dormancy.
