Table 2.
Reproductive deficiencies observed in clock genes mutants mice.
| Clock gene | Gender | Mutation | Reproductive deficiencies |
|---|---|---|---|
| Clock | Female | ClockΔ19 | Irregular and lengthened estrous cycles, ↑ fetal reabsorption and term-pregnancy failures, interferes with coordinated release of GnRH, abnormal LH secretion patterns, affects maternal behavior, growth, litter size, and survival of pups (96, 110–112) |
| Male | ClockΔ19 | No significant difference in male fecundity (110, 112) | |
| Bmal1 | Female | Bmal1−/− | Infertile following sub-developed reproductive organs, abnormal estrous cycles, ↓ progesterone synthesis (108, 113–115) |
| Male | Bmal1−/− | ↑ LH levels, ↓ testosterone levels, impaired steroidogenesis, and accelerated reproductive aging (108, 115) | |
| Per1/Per2 | Female | Per1−/− and Per2−/− | No signs of reproductive instability in young adult stages; mid-aged mutants have prolonged and acyclic estrous cycles (116) |
| Male | – | No available literature on male rodents |
Bmal1, Brain and muscle ARNT-like 1; Clock, Circadian locomotor output cycle kaput; FSH, follicle-stimulating hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; and Per, period.