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Generation of myometrium-specific Bmal1 knockout mice for parturition analysis
Christine K Ratajczak1, Minoru Asada, Gregg C Allen
1Molecular Cell Biology Program, Washington University, St Louis, MO 63110, USA.
Reproduction, Fertility, and Development
|June 16, 2012
Summary
Disrupting the Bmal1 clock gene in the myometrium, the uterine muscle, delayed normal parturition timing in mice. Myometrial Bmal1 is crucial for maintaining the expected time of birth.
Area of Science:
- Reproductive Biology
- Chronobiology
- Molecular Genetics
Background:
- Circadian rhythmicity and clock gene expression are vital for normal parturition.
- The role of clock genes outside the suprachiasmatic nucleus is an emerging area of research.
Purpose of the Study:
- To investigate the function of the Bmal1 clock gene within the myometrium during parturition.
- To determine if myometrial Bmal1 influences the timing of birth.
Main Methods:
- Utilized a Bmal1 conditional knockout mouse model.
- Employed a novel Cre transgenic mouse line to disrupt myometrial Bmal1.
- Monitored parturition timing and analyzed serum progesterone and uterine gene expression.
Main Results:
- Females with disrupted myometrial Bmal1 showed a reduced success rate in completing parturition within the normal time window (64% vs. 92% in controls).
- No significant differences were observed in serum progesterone levels or uterine expression of Connexin43 and Oxytocin receptor between groups.
Conclusions:
- Myometrial Bmal1 plays a significant role in regulating the time of day of parturition.
- While Bmal1 affects parturition timing, it does not appear to influence progesterone levels or key contractile-associated protein expression in late gestation.
