Abstract: Oxygen deprivation (anoxia or hypoxia) is central to the pathology of various medical problems (heart attack, stroke, solid tumor cancer cells) leading to severe economic and human health consequences. Many organisms can survive oxygen deprivation, and it is of interest to study the mechanisms they employ to do this. The soil nematode Caenorhabditis elegans can survive one day of anoxia, and mutations in the daf-2/daf-16 pathway can increase this length of time (Padilla, Nystul, Zager, Johnson, & Roth, 2002; Mendenhall, LaRue, & Padilla, 2006). I investigated daf-2mutants in anoxia and found that mutations in the ligand binding site of Class 1 mutants allowed C. elegans to survive long term anoxia at very high rates. Additionally, I was interested in seeing if expression of the DAF-16 transcription factor in certain tissues would increase C. elegans anoxia survival as it was shown to increase lifespan when expressed in the intestine (Libina, Berman, & Kenyon, 2004). Unlike longevity, expression of DAF-16 only increased anoxia survival when expressed in the neurons as compared with DAF-16 in the muscle or intestine. These findings provide an understanding for the development of anoxia-related therapies in humans, and genetic treatments of human diseases.
