Mentor: Nina Tang Sherwood, Ph.D.
Department of Biology
The SPG4 (spastin) gene plays a role in microtubule severing, and when mutated in humans, it causes Autosomal Dominant Hereditary Spastic Parapelgia (AD-HSP), a disease that impairs mobility in the legs. Previous studies in Drosophila have shown that ubiquitous spastin deletion creates small, bunched boutons in the larval neuromuscular junction (NMJ) and motor defects in surviving adults. However, it remains unknown where spastin acts. We are testing the hypothesis that spastin acts in a specific tissue, such as neurons or glia. To test this, we are using CRISPR-Cas9P2 and a tissue-specific expression system to delete spastin exclusively in the glia and neurons of Drosophila. Additionally, we are examining flies with ubiquitous spastin deletion to control for the novelty of the Cas9P2 technology in Drosophila spastin. If Spastin is acting in a tissue-specific manner, the flies with the tissue-specific deletion will show the spastin mutant phenotype. In addition to studying the site specificity of Spastin, this study aims to test the effectiveness of Cas9P2 as a genome editing tool in Drosophila and contribute to the knowledge base of those studying AD-HSP.