"Deciphering Neuronal Expression and Behavioral Consequences of Dys-1b " by Shifat Niha

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Graduation Term

Spring 2025

Degree Name

Master of Science (MS)

Department

School of Biological Sciences

Committee Chair

Andres Vidal-Gadea

Committee Member

Wolfgang Stein

Committee Member

Martin Engelke

Abstract

Duchenne Muscular Dystrophy (DMD) is a progressive muscle degenerative disease often accompanied by a range of neurological impairments including epilepsy, ADHD, depression, reading disability, autism, etc. The cause of DMD is mutations in the gene encoding several isoforms of dystrophin proteins expressed in both muscles and neurons. In muscles, dystrophin plays a critical role in maintaining the structural stability of the muscle fiber. However, the precise function of dystrophin in sensory neurons remains unknown. C. elegans homolog of human dystrophin, dys-1 has been used to study DMD for decades. The goal of this study is to generate a better understanding of the function of dystrophin in the sensory neurons using C. elegans and identify how the loss of dystrophin leads to disease-associated sensory impairments. I show that two sensory neurons in C. elegans ASH and ADE express dys-1b and dys-1e, respectively. The loss of dys-1 resulted in impaired ASH- and ADE-dependent responses to stimuli, while rescue of dys-1b and dys-1e restored the neuron-specific behavioral deficits observed in the dystrophic animals. My results suggest that dys-1 is necessary to maintain proper sensory functions of ASH and ADE neurons in C. elegans. Dys-1e rescued some of the ASH-dependent behaviors in the dys-1 knockout background, suggesting that each isoform likely contributes to neuronal function through different mechanisms. This master’s thesis contributes to our understanding of how the loss of dys-1 contributes to the recognized sensory neurological phenotypes associated with Duchenne Muscular Dystrophy.

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Available for download on Friday, June 26, 2026

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