Loss-of-function mutations with circadian rhythm regulator Per1/Per2 lead to premature ovarian insufficiency†. Issue 4 (18th November 2018)

• Record Type: Journal Article
• Authors: Zheng, Yating; Liu, Chao; Li, Yan; Jiang, Haijuan; Yang, Peixin; Tang, Jing; Xu, Ying; Wang, Han; He, Yulong
• Is Part Of: Biology of reproduction. Volume 100:Issue 4(2019)
• Page Start: 1066
• Page End: 1072
• Publication Date: 2018-11-18
• Subjects: PER1 -- PER2 -- ovarian follicle -- ovarian insufficiency -- knockout mouse; Reproduction -- Periodicals; Biology; Reproduction; Reproduction; Electronic journals; Periodicals; Periodicals; 571.805
• DOI: 10.1093/biolre/ioy245
• Languages: English
• ISSNs: 0006-3363

Abstract

Abstract: The mechanism underlying premature ovarian insufficiency remains incompletely understood. Here we report that mice with Per1 m/m ; Per2 m/m double mutations display a decrease in female fertility starting approximately at 20 weeks old, with significantly less pups born from 32 weeks old onwards. Histological analysis revealed that a significant reduction of ovarian follicles was observed in the Per1/Per2 mutants compared with the littermate controls examined at 26 and 52 weeks old, while the difference was not statistically significant between the two groups at 3 and 8 weeks old. We further showed that vascular development including the ovarian follicle associated vascular growth appeared normal in the Per1/Per2 mutant mice, although clock genes were reported to regulate angiogenesis in zebrafish. The findings imply that loss-of-function mutations with Per1/Per2 result in a premature depletion of ovarian follicle reserve leading to the decline of reproductive capacity. Abstract : Disruption of circadian rhythm or its underlying regulatory network contributes to the premature depletion of ovarian follicle reserve.