2004 Midwest Worm Meeting abstract 57
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Department of Biological Sciences, University of North Texas, Denton, TX 76203
A variety of organisms have adapted mechanism to survive oxygen deprivation. C. elegans, at all stages of their life cycle, are capable of surviving at least one day of anoxia. Embryos exposed to anoxia enter into a state of suspended animation in which there is an arrest of developmental and cell cycle progression. These embryos are capable of surviving anoxia for at least three days. We are interested in understanding the molecular mechanisms C. elegans use to survive oxygen deprivation. Analysis of chromosomal, microtubule, and kinetochore structure in blastomeres of embryos exposed to anoxia was done to investigate the signaling pathway between low oxygen concentrations and cell cycle arrest. Previously, the spindle checkpoint genes, san-1 and mdf-2, were identified to be required for embryonic anoxia survival. Further phenotype analysis of san-1 (RNAi) and mdf-2 (RNAi) was conducted to understand the signaling pathway from low oxygen concentrations to spindle checkpoint activation. A histone::GFP strain was used to analyze chromosome segregation in N2, san-1 (RNAi) and mdf-2 (RNAi) embryos exposed to anoxia. Additionally, SAN-1 localization in embryos exposed to anoxia was examined and results indicate that the localization is altered in embryos exposed to anoxia. An understanding of how C. elegans survive oxygen deprivation will lead to a greater understanding of the metazoan response to oxygen deprivation and how embryonic development and cell cycle progression is effected by environmental changes.