Date of Award

12-2013

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Legacy Department

Environmental Toxicology

Committee Chair/Advisor

Dr. William S. Baldwin

Committee Member

Dr. Stephen J. Klaine

Committee Member

Dr. Cindy M. Lee

Committee Member

Dr. Peter Van Den Hurk

Committee Member

Dr. Robert S. Cohen

Abstract

Healthy reproduction and neonatal sex ratios of Daphnia are crucial to the health of the aquatic ecosystems in which Daphnia play principal roles in trophic transfer of nutrients. Combinations of environmental factors such as availability and quality of diet, overcrowding, hypoxia, reduced photoperiods and fall in ambient temperatures perturb normal parthenogeneic reproduction and induce sexual reproduction through male production. Male production provides a mechanism for overcoming specific stressors such as overcrowding and overwinter pond desiccation. However, it also induces a decrease in the Daphnia population that could have adverse implications on the pond ecosystem that depend on Daphnia . Interestingly, Daphnia exhibit great phenotypic and reproductive plasticity in response to different environmental stressors. I hypothesized that arachidonic acid (AA), a dietary ω-6 fatty acid that accumulates in the ovary of Daphnia influences Daphnia reproduction and is important in counteracting the male production effects induced by environmental stressors. In this study, I investigated the male production effects of a juvenile hormone analog, the insecticide pyriproxyfen in Daphnia magna and examined how a diet rich or poor in arachidonic acid influences overall fecundity and amelioration of pyriproxyfen mediated sex ratio. Further investigation is focused on the novel nuclear hormone receptor HR97g. Based on higher expression of HR97g in the ovaries of mature Daphnia and inhibition by arachidonic acid in vitro, I thought that interactions of AA and HR97g are important in regulation of neonatal sex ratios. However, HR97g is only partially activated by pyriproxyfen in vivo and the significance of their interaction needs to be determined. In addition, AA is metabolized to eicosanoids and I hypothesized that these molecules may play a role in male production. However, ibuprofen inhibition of AA did not perturb male production, but it did induce selective developmental abnormalities. In conclusion, pyriproxyfen is a juvenile hormone pesticide that induces male production in a time-dependent manner, and AA can in part ameliorate this activity as a potent dietary activator of fecundity.

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