|Greenlee, Kendra - North Dakota State University|
|Bowsher, Julia - North Dakota State University|
|Heidinger, Britt - North Dakota State University|
|Rinehart, Joseph - Joe|
Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 3/22/2017
Publication Date: 4/22/2017
Citation: Greenlee, K.J., Bowsher, J.H., Heidinger, B., Rinehart, J.P., Yocum, G.D. 2017. Mechanisms of increased lifespan in hypoxia. Federation of American Societies for Experimental Biology Conference. 31:1075.8.
Technical Abstract: Genetic variation accounts for a relatively small amount of the variation in lifespan (generally 15-30%), while environmental stressors are very strong predictors (Finch and Kirkwood 2000). Hypoxia is an environmental stress that increases longevity in some contexts, but the mechanisms remain poorly understood. Our long-term goal is to understand the mechanisms by which hypoxia extends lifespan. In the bee Megachile rotundata, lifespan doubles upon rearing in hypoxia (Abdelrahman et al. 2014). We hypothesize that that hypoxia increases longevity by limiting telomere loss from reactive oxygen species (ROS). In this study, prepupal bees were maintained in 10, 21 or 24% oxygen for 9 months. Each month, two subsets of bees were removed. One group was immediately frozen for processing. A second subset of bees was reared to adulthood and then frozen for processing. Similar to our previous findings, all bees had extended lifespans compared to bees in the wild, but bees exposed to hypoxia had high survival after 9 months in 10% oxygen. At nine months, bees reared in 24% oxygen had 14% survival, while those in normoxia had 41% survival. Because they survived better than bees in normoxia or hyperoxia, we predicted that bees in hypoxic conditions would have reduced telomere loss rates, lower levels of ROS, and/or higher levels of telomerase activity than bees exposed to normoxia. We measured total antioxidant activity and found no differences among treatments from either prepupal or adult bees, indicating that oxidative stress is not regulated at the level of antioxidants. Because antioxidants are invariant, we predict that increased oxidative damage to proteins will be observed under normoxic and hyperoxic conditions. We expect bees reared in hypoxia to have longer telomeres than bees reared in normoxia or hyperoxia. In addition, we expect bees reared in hypoxia to have lower levels of oxidative damage than bees reared in normoxia or hyperoxia.