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dc.contributor.authorZheng, Y.
dc.contributor.authorLiu, C.
dc.contributor.authorLi, Y.
dc.date.accessioned2019-09-13T16:41:58Z
dc.date.available2019-09-13T16:41:58Z
dc.date.issued2019
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85068538072&doi=10.1093%2fbiolre%2fioy245&partnerID=40&md5=23b8069535ebb610af511418462a2486
dc.identifier.urihttp://hdl.handle.net/10713/10679
dc.description.abstractThe 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. Copyright The Author(s) 2018.en_US
dc.description.urihttps://doi.org/10.1093/biolre/ioy245en_US
dc.language.isoen-USen_US
dc.publisherOxforden_US
dc.relation.ispartofBiology of reproduction
dc.subjectknockout mouseen_US
dc.subjectovarian follicleen_US
dc.subjectovarian insufficiencyen_US
dc.subjectPER1en_US
dc.subjectPER2en_US
dc.titleLoss-of-function mutations with circadian rhythm regulator Per1/Per2 lead to premature ovarian insufficiencyen_US
dc.typeArticleen_US
dc.identifier.doi10.1093/biolre/ioy245
dc.identifier.pmid30452546


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