PUBLICATION
Loss-of-function mutations with circadian rhythm regulator Per1/Per2 lead to premature ovarian insufficiency
- Authors
- Zheng, Y., Liu, C., Li, Y., Jiang, H., Yang, P., Tang, J., Xu, Y., Wang, H., He, Y.
- ID
- ZDB-PUB-181127-10
- Date
- 2018
- Source
- Biology of reproduction 100(4): 1066-1072 (Journal)
- Registered Authors
- Liu, Chao, Li, Yan, Wang, Han
- Keywords
- none
- MeSH Terms
-
- Animals
- Circadian Rhythm/genetics
- Female
- Infertility, Female/genetics
- Loss of Function Mutation*
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Transgenic
- Ovarian Reserve/genetics
- Period Circadian Proteins/genetics*
- Primary Ovarian Insufficiency/genetics*
- Primary Ovarian Insufficiency/pathology
- PubMed
- 30452546 Full text @ Biol. Reprod.
Citation
Zheng, Y., Liu, C., Li, Y., Jiang, H., Yang, P., Tang, J., Xu, Y., Wang, H., He, Y. (2018) Loss-of-function mutations with circadian rhythm regulator Per1/Per2 lead to premature ovarian insufficiency. Biology of reproduction. 100(4):1066-1072.
Abstract
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-week-old, with significantly less pups born from 32-week-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-week-old while the difference was not statistically significant between the two groups at 3- and 8-week-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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping