Meeting Abstract
P2.111 Thursday, Jan. 5 Metabolic Downregulation in Embryos of Artemia franciscana during Diapause PATIL, Y.N.*; BOSWELL, L.; MARDEN, B.; HAND, S.C.; Louisiana State University, Baton Rouge, LA 70803; Louisiana State University, Baton Rouge, LA, 70803; Great Salt Lake Artemia LLC, Ogden, UT, 84401; Louisiana State University, Baton Rouge, LA, 70803 ypatil1@lsu.edu
Artemia franciscana embryos characteristically display a low metabolic rate in the diapause state. We have confirmed this observation for embryos released from ovigerous females collected from the Great Salt Lake, Utah. Metabolic rate as judged by respiration is depressed acutely across a 26-day time course. We measured selected metabolic intermediates in diapause and post-diapause embryos in order to identify sites of inhibition in the metabolic pathway from trehalose to acetyl-CoA. Based on the values obtained for product to substrate ratios, we calculated a strong negative crossover point for hexokinase in diapause (glucose-6-phosphate/glucose; 0.045 ± 0.0009; ± SE, n = 6) as compared to the post-diapause state (0.759 ± 0.005). A second inhibition point was observed at pyruvate kinase in diapause (pyruvate/phosphoenol pyruvate; 0.150 ± 0.009; ± SE, n = 4) versus the post-diapause state (0.624 ± 0.048). Finally, a third inhibition was observed at pyruvate dehydrogenase (PDH) in diapause (acetyl CoA/pyruvate; 0.013 ± 0.0012; ± SE, n = 6) as compared to the post-diapause state (0.042 ± 0.0028). These inhibitions are consistent with a restriction of carbohydrate fuel to the mitochondrion. We quantified the phosphorylation state of site 1 for PDH subunit E1 α (pPDH) in diapause and post-diapause embryos. The relative amount of pPDH was higher in diapause embryos as compared to post-diapause embryos, which suggests that the PDH in diapause may be inhibited. Taken together, the findings indicate that substrate availability for oxidative phosphorylation plays a crucial role in downregulating metabolic rate during diapause. (Supported by NSF grant IOS-0920254)
