The later years of life are often characterized by declining cognitive function and mobility. One contributor is the cellular accumulation of reactive oxygen species (ROS). However, our understanding of how cells respond to ROS to promote health and survival is incomplete. We focused here on two genes, follicle stimulating hormone receptor-1 (fshr-1) and sphingosine kinase-1 (sphk-1), encoding proteins that mediate responses to oxidative stress and regulate life history traits, including lifespan and brood size, as well as neuromuscular function, in the roundworm C. elegans. Both genes are conserved in humans where they are similarly implicated in stress responses, cellular survival, and neuronal functions. Interestingly, fshr-1 and sphk-1 work together to mediate responses to intestinal oxidative stress. Whether these genes work in a common pathway to control lifespan or brood size is unknown. Our recent findings indicate potential phenotypic differences in life history traits based on the bacterial food source for the worms. The typical food source, OP50 E. coli, is pathogenic compared to the alternative HB101 strain. We hypothesized differences in pathogenicity between the two bacteria strains causes decreased lifespan and brood size through oxidative stress effects that may differentially affect sphk-1 and fshr-1 mutants. We found fshr-1 is required for normal lifespan and brood size in C. elegans and confirmed the pathogenicity levels of the bacterial lawns did not significantly impact on these traits. Tests for effects on sphk-1 mutants are ongoing as are experiments testing the activity of these genes in a common pathway for life history regulation.
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Ryan is an undergraduate at Butler University studying biology and biochemistry. He is from Twinsburg, Ohio Ryan is also a staff editor for research and politics at The University Journal.