Date of Award

2017

Document Type

Thesis

Department

Science

First Advisor

David B. Morton

Subjects

Exons (Genetics), Amyotrophic lateral sclerosis -- Genetics, DNA-binding proteins, Drosophila -- Genetics

DOI

10.15760/honors.419

Abstract

Defects in the TAR DNA-binding protein named TDP-43 are known to be involved with many neurodegenerative diseases, including ALS. TBPH, a TDP-43 Drosophila orthologue is used to explore the specifics of those defects. This protein is known to have many cellular roles, one of them being a regulator for splicing. TBPH null flies have shown that the region coding for the voltage gated calcium channel cacophony is a potential target for splicing, directly producing a greater number of transcripts that lack exon 7. In this report, the phenotype of adult flies that lack exon 7 is explored. These mutants are known to have reduced larval crawling and decreased expression of cacophony. In this study exon 7(-) adult flies exhibit reduced activity compared to wild type flies as well as a decreased ability to survive exposure to caffeine. These phenotypes were rescued by a duplication of the cacophony genome. Driving cacophony selectively in neurons with different UAS-GAL4 drivers as a followup experiment is discussed with preliminary data.

Comments

An undergraduate honors thesis submitted in partial fulfillment of the requirements for the degree of Bachelor of Science in University Honors and Science.

Persistent Identifier

http://archives.pdx.edu/ds/psu/20421

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