Sumoylation Inhibition in Sertoli Cells Reduces Cell Viability via Apoptosis.
Description
senior honors thesis
Abstract
Male Infertility affects 15% of couples worldwide and is a contributing factor to about
50% of cases of infertility. While sometimes attributed to certain environmental factors and
genetic mutations, many cases of infertility require a deeper understanding of
spermatogenesis and the necessary enzymes that promote its progression in order to diagnose
and treat effectively. Recent studies have explored the unique SUMO (small ubiquitin-like
modifier) protein and how it modifies post-translational proteins by sumoylation in a variety
of ways. Our lab has focused on its role within the various cells in the male testes. In this
study, we sought to determine importance of sumoylation specifically in the supportive
somatic cells found in the testes, known as sertoli cells. Sertoli cells are known to provide
nutritional, mechanical and immune support toward differentiating cells during
spermatogenesis. In each experiment, we treated sertoli cell lines with the sumoylation
inhibitor, ginkgolic acid at varying concentrations and analyzed the resultant cell fate. A
WST-1 viability assay revealed that sertoli cells shut down when sumoylation was inhibited.
Furthermore, we identified apoptosis as the particular mode of cell death initiated by these
cells lacking sumoylation ability. Sumoylation, however, was not proven necessary for the
proliferation of sertoli cells, which was not affected by the addition of ginkgolic acid. Future
studies will explore more specific identification of SUMO targets in sertoli cells and which
directly activate apoptosis.
Permanent Link(s)
https://hdl.handle.net/20.500.12202/6071Citation
Schwartz, Tamar. (August 14, 2020). Sumoylation Inhibition in Sertoli Cells Reduces Cell Viability via Apoptosis. Presented to the S. Daniel Abraham Honor’s Program in Partial Fulfillment of the Requirements of Completion of the Program Stern College for Women Yeshiva University. Mentor: Dr. Margarita Vigodner, Cell Biology
*This is constructed from limited available data and may be imprecise.
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