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Editor's Notes

Ashley Munie graduated from Murray State in the spring of 2017 with a BS in Biology and Biomedical Science. This is her senior Honors thesis, which was completed as a partial requirement for the Murray State Honors Diploma. She was mentored by Dr. Chris Trzepacz. An interview about her research process can be viewed in the previous issue of Steeplechase.

Abstract

Autophagy, the cell's recycling system, is a highly-conserved survival mechanism of the cell. Autophagy has been implicated in the mediation of the removal of cytotoxic aggregates, such as those linked to neurodegenerative disorders like Huntington and Alzheimer disease. Studies in several model organisms have identified numerous genes involved in mediating autophagy, including the Puromycin sensitive aminopeptidase (Psa). The Caenorhabditis elegans orthologue of Psa, pam-1, also governs fertility. Along with apoptosis, a form of regulated cell death, autophagy has been found to be required for efficient C. elegans oogenesis. When autophagy is suppressed through RNAi in worms harboring a pam-1 mutation, pam-1 influenced fertility defects are exacerbated in this study. The involvement of PAM-1 in the autophagic regulation of oogenesis has been investigated through construction and examination of a GFP::pam-1 transgenic strain. The localization of PAM-1 during autophagic suppression and autophagic stimulation were also examined. Our results provide insight into autophagic regulation of C. elegans oogenesis, and by extension, these processes in higher eukaryotes including humans.

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