Sarah Clark

Background & Contact Information

Position (2024 – Present)
Education: BS University of Richmond  Biology with a concentration in Neuroscience
Fellowships & Awards: Spring 2024 Biology Teaching Assistant Award
Email: sarclark@unc.ed

Screenshot

Research Information
Prior to joining the Peifer Lab, I studied at the University of Richmond where I worked in the research lab of Dr. John M. Warrick studying neurodegenerative disease mechanisms in a Drosophila model. My project focused on examining the influence of the Histone Acetyltransferase Tip60 expression on cellular and motor degeneration in Drosophila modeling Machado-Joseph Disease.

 

Following graduation, I wanted to expand my biological knowledge and skillset, so I joined the Peifer Lab. Since joining the Peifer Lab, I have worked closely with postdoc Dr. Maik Bischoff on furthering our scientific understanding of collective cell migration. We use a novel collective cell migration model where nascent myotubes migrate over the Drosophila testes. In order to identify regulators of testis nascent myotube migration, a large-scale candidate RNAi screen was conducted based on Maik’s testis nascent myotube RNAseq dataset. My work primarily focuses on the in vivo and ex vivo analysis of testis nascent myotube migration in Drosophila lacking or over-expressing gene candidates identified in the screen.
One notable hit in the screen was the receptor Plexin A (PlexA). PlexA knockdown leads to significant defects in the muscle coverage of the adult testes. Semaphorins are ligands that bind to the Plexin family, and the knockdown of Sema1b yields a similar adult phenotype to PlexA. Plexins and Semaphorins have been shown to regulate contact dependent axon-axon repulsion, making them a crucial set of regulators to study in the collective cell migration process. Currently, I am using live cell imaging techniques on a spinning disc microscope to examine defects in collective cell migration in testes with reduced PlexA expression. These images will be analyzed along with testes expressing Sema1b knockdown, in order to define on the role and mechanism of PlexinA/Semaphorin signalling on effective collective cell migration.
Another notable hit in the screen was the Guanine Nucleotide Exchange Factor (GEF) Pix. Pix is known to regulate Cdc42 and Rac, which are molecules that mediate crucial processes in cell migration, such as filopodia formation and matrix adhesion. Knockdown of Pix in adult testis revealed strong defects in myotube migration and a potential over adhesion phenotype. NCadherin, another important cell adhesion molecule, is known to promote adhesion in testis nascent myotubes . Currently, I am investigating the potential roles of Pix in collective cell migration, both individually and in conjunction with NCadherin. I do this by imaging testes using confocal microscopy and subsequently analyzing testes nascent myotube gaps in the adult testes using ImageJ software.
Publications
Maik C. Bischoff, Jenevieve E. Norton, Erika A. Munguia, Noah J. Gurley, Sarah E. Clark, Rebecca Korankye, Emmanuel Addai Gyabaah, Taino Encarnacion, Christopher J. Serody, Corbin D. Jones, and  Mark Peifer (2024) A large reverse genetic screen identifies numerous regulators of testis nascent myotube collective cell migration and collective organ sculpting.  BioRxiv.  https://www.biorxiv.org/content/10.1101/2024.10.10.617659v1

 

 

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