Date on Honors Thesis

Spring 5-2024

Major

Biology/Pre-Medical

Minor

Chemistry

Examining Committee Member

Dr. Chris Trzepacz, Advisor

Examining Committee Member

Dr. Dena Weinberger, Committee Member

Examining Committee Member

Dr. J. Ricky Cox, Committee Member

Abstract/Description

The deteriorating effects of neurodegenerative conditions seem inescapable for many as they age. The experimental exploration of the molecular and cellular mechanisms responsible for neurodegeneration is aided using animal models. For instance, genetic screens have identified the puromycin-sensitive aminopeptidase (PSA) as a novel effector of neurodegeneration, as mutations in PSA in fruit flies result in perturbations of neuron anatomy and an accelerated onset of neuron death. We have tested the hypothesis that PAM-1, the Caenorhabditis elegans ortholog of PSA, plays a similar role in governing neurodegeneration in nematodes. Genetic strains were created that express the green fluorescent protein (GFP) in the six mechanosensory neurons of wild-type and pam-1 mutant C. elegans. Because C. elegans is transparent, each of these GFP-labeled strains produce animals that brilliantly illuminate the invariant position, anatomy, and neurodegeneration of a specific subset of neurons. The degeneration can be seen as a natural consequence of aging in the wild-type worms. In the pam-1 mutant worms, however, a higher prevalence and earlier appearance of similar defects is witnessed. Additionally, it seems that the mutated worms have a shorter lifespan than their wild-type counterparts. The pam-1 mutation, its effects, and the research done with C. elegans sheds light on neurodegeneration in a manner impossible for human subjects.

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