Zebrafish gsdf mutant provides a disease model for human polycystic ovary syndrome
dc.contributor.advisor | Postlethwait, John | en_US |
dc.contributor.author | Liu, Jiawei | en_US |
dc.date.accessioned | 2017-06-09T18:28:08Z | |
dc.date.available | 2017-06-09T18:28:08Z | |
dc.description | Single page poster | en_US |
dc.description.abstract | Polycystic ovary syndrome (PCOS) is the most frequent problem when a couple comes to a fertility clinic. PCOS in women includes the accumulation of premature oocytes in ovaries. We discovered that zebrafish lacking activity of the gsdf gene (gonad soma derived factor) due to gene editing (TALENS) mimic the pathology of PCOS. Homozygous gsdf mutants have delayed differentiation of the bi-potential gonad to ovary or testes during gonad development accumulation of young oocytes, elevated androgen, premature loss of fertility, obesity, and inappropriate expression of genes for lipid metabolism and insulin. We conclude that the gsdf mutant in zebrafish provides a disease model for human PCOS and suggests pathways for potential therapies. | en_US |
dc.identifier.uri | https://hdl.handle.net/1794/22383 | |
dc.rights | Creative Commons BY-NC-ND 4.0-US | en_US |
dc.subject | Undergraduate Research Symposium | en_US |
dc.title | Zebrafish gsdf mutant provides a disease model for human polycystic ovary syndrome | en_US |