Student Theses and Dissertations

Date of Award

Spring 5-2-2025

Document Type

Thesis

Degree Name

B.A.

Honors Designation

yes

Program of Study

Biology

Language

English

First Advisor

Krista C. Dobi

Second Advisor

Rebecca Spokony

Abstract

Muscle atrophy is a result of a number of muscle diseases, as well as aging, disuse, and infections. Muscles weakened in these ways exhibit a characteristic decrease in size, strength, and mobility. The similarities between muscle in humans and Drosophila allow for direct comparisons to be made in vertebrates from studying muscle in Drosophila. Differential gene expression has been shown to play an important role in embryonic muscle development in Drosophila melanogaster. A previous study identified Elongin B (EloB) to be involved in somatic muscle morphogenesis in Drosophila, with mutant embryos displaying severe muscle defects, including thin, mis-attached, and missing myofibers. However, there is still a gap in knowledge regarding how exactly EloB contributes to muscle development. The high conservation of the EloB protein between Drosophila and humans is cause for investigation into how exactly the observed muscle phenotypes are obtained. EloB expression and embryonic muscle morphology were examined by immunohistochemistry, using antibodies to EloB and myosin heavy chain, respectively. In these experiments, embryos were fixed, stained, and imaged with confocal microscopy to visualize muscle defects. High expression of EloB was found in the dorsal pharyngeal musculature in stage 16 embryos. After visualizing the muscle pattern in both transposon insertion and RNAi knockdown mutant embryos, numerous muscle defects were observed within the somatic muscle pattern including missing and misattached muscles, unfused myoblasts and mesodermal patterning defects. Interestingly, overexpression of EloB did not result in any major defects. These results underscore the important role of EloB in somatic muscle development.

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