An increasing number of women delay childbearing and consequently face infertility and pregnancy complications associated with age. The central contributor to compromised reproductive performance is poor oocyte quality. Despite advances in assisted reproductive technologies, a strategy to overcome the damage that oocytes receive with age is yet to be identified. This work focuses on the influence of TAp73, a protein that decreases in mouse and human eggs with age, on the developmental capacity of mouse oocytes. TAp73 deficient mice were found to have fewer active mitochondria and compromised clearance of damaged material in their oocytes, possibly due to reduced mTOR-TAp73 axis signaling. These qualities were shown to contribute to low oocyte maturation rates. Additionally, TAp73 likely mediates the action of coenzyme Q10, which restores oocyte TAp73 levels and mitochondrial quality in aged mice. Together these findings suggest that TAp73 is a promising therapeutic target for improving oocyte function.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:OTU.1807/42427 |
Date | 15 November 2013 |
Creators | Yavorska, Tetyana |
Contributors | Jurisicova, Andrea |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | en_ca |
Detected Language | English |
Type | Thesis |
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