| First Author | Zheng Y | Year | 2019 |
| Journal | Biol Reprod | Volume | 100 |
| Issue | 4 | Pages | 1066-1072 |
| PubMed ID | 30452546 | Mgi Jnum | J:277649 |
| Mgi Id | MGI:6316895 | Doi | 10.1093/biolre/ioy245 |
| Citation | Zheng Y, et al. (2019) Loss-of-function mutations with circadian rhythm regulator Per1/Per2 lead to premature ovarian insufficiency. Biol Reprod 100(4):1066-1072 |
| abstractText | The mechanism underlying premature ovarian insufficiency remains incompletely understood. Here we report that mice with Per1m/m; Per2m/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. |
