Semester of Graduation

Spring 2026

Degree

Master of Science (MS)

Department

Biological Sciences

Document Type

Thesis

Abstract

This study tested the hypothesis that downregulation of mitochondrial Complex I may contribute to the metabolic depression during diapause in embryos of Artemia franciscana. Embryos of this extremophile exhibit strong metabolic depression during anoxia and diapause (a programmed arrest of development and metabolism controlled by endogenous physiological factors). Catalytic activity of Complex I was measured with an assay for NADH-ubiquinone oxidoreductase activity, and the quantity of Complex I (specifically, the amount of flavin site) was assessed with the NADH:APAD+ assay. Surprisingly, the quantity and activity of Complex I were two-fold higher during diapause compared to post-diapause. Artificial termination of diapause with H2O2 treatment promoted the lowering of both Complex I quantity and activity. Virtual identical patterns for the catalytic activity and the flavin site quantity of Complex I across diapause and post-diapause states suggest the upregulation of Complex I is due to increased amount of Complex I, i.e., the activity simply follows the increased quantity. Thus, my hypothesis that Complex I activity and quantity would be downregulated during diapause, as a contributing mechanism to metabolic depression, was proven incorrect. The physiological role of this novel increase in Complex I during diapause in embryos of A. franciscana is unclear, but it possibly could be a mechanism contributing to metabolic reinitiation upon diapause termination.

Date

3-25-2026

Committee Chair

Hand, Steven C

LSU Acknowledgement

1

LSU Accessibility Acknowledgment

1

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Available for download on Sunday, March 25, 2029

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