| First Author | Ratajczak CK | Year | 2009 |
| Journal | Endocrinology | Volume | 150 |
| Issue | 4 | Pages | 1879-85 |
| PubMed ID | 19056819 | Mgi Jnum | J:151819 |
| Mgi Id | MGI:4355306 | Doi | 10.1210/en.2008-1021 |
| Citation | Ratajczak CK, et al. (2009) Impaired steroidogenesis and implantation failure in Bmal1-/- mice. Endocrinology 150(4):1879-85 |
| abstractText | Evidence in humans and rodents suggests that normal circadian rhythmicity is important for supporting reproductive function. A molecular clock underlies circadian rhythmicity. Impaired fertility is observed in some genetically altered mice with deficiencies in genes of the molecular clock, suggesting a critical role for these genes in reproduction. Here we systematically characterize the reproductive phenotype of females deficient in the clock gene Bmal1. Bmal1(-/-) females are infertile. They exhibit progression through the estrous cycle, although these cycles are prolonged. Normal follicular development occurs in Bmal1(-/-) females, and healthy embryos of the expected developmental stage are found in the reproductive tract of Bmal1(-/-) females 3.5 d after mating to wild-type males. However, serum progesterone levels are significantly lower in Bmal1(-/-) vs. Bmal1(+/+/-) females on d 3.5 of gestation. Low progesterone levels in Bmal1(-/-) females are accompanied by decreased expression of steroidogenic acute regulatory protein in corpora lutea of Bmal1(-/-) vs. Bmal1(+/+/-) females. Whereas implantation of embryos is not observed in untreated or vehicle-treated Bmal1(-/-) females, exogenous administration of progesterone to Bmal1(-/-) females is able to reinstitute implantation. These data suggest that implantation failure due to impaired steroidogenesis causes infertility of Bmal1(-/-) females. |
