Graduation Year

2026

Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts

Department

Neuroscience

Reader 1

Sandra Watson

Reader 2

Thomas Borowski

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© 2026 Saenger M Breen

Abstract

Dopamine (DA) is a highly conserved neuromodulator that regulates locomotor activity and sleep-wake rhythms, and Drosophila melanogaster offer a strong genetic system for investigating DA-dependent behavior. The brain tumor (brat) gene, located within the Dopa decarboxylase (Ddc) gene cluster, encodes the tumor suppressor TRIM-NHL, hypothesized to be involved in neural progenitor proliferation, catecholamine regulation, and brain architecture. Previous work on Ddc gene cluster mutants asserts that a loss of brat increases concentrations of DA and its related metabolites, prompting the hypothesis that a reduction in brat may disturb DA homeostasis and change DA-dependent behaviors, when L-DOPA/carbidopa (LDC) treatment induces increased DA synthesis. This thesis seeks to investigate brat’s effects on DA-dependent locomotor activity and sleep, utilizing brat glial knockdown (repo-GAL4 > UAS-brat RNAi) and a respective control (repo-GAL4 > UAS-RNAi), with phenotypic behavior analyzed with Drosophila Activity Monitor (DAM) assays. Both at baseline and LDC conditions, there were no clear differences in glial brat knockdown and control fly locomotor activity, suggesting that brat changes localized to glia do not generate pronounced DA-dependent locomotor phenotypes. LDC treatment in both glial genotypes shifted the timing of sleep toward the dark phase, reduced daytime sleep fractions, but did not alter the nighttime sleep fractions, which remained high. Overall, the data show that LDC reduces total sleep in the control genotype, and produces a sub-threshold reduction in the glial brat knockdown. The data propose that, due to the lack of apparent, brat dependent differences within the control and experimental glial RNAi lines, a decrease in glial brat does not initiate robust DA-dependent activity or sleep phenotypes. This instead suggests that brat’s involvement in DA-associated modulation is diffuse and dispersed across various tissues, and most significantly impacts other neurons or non-glial cell types.

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