Research On The Maternal Effects On Puberty Onset Timing In Mice Offspring

Puberty, which is characterized by complicated biologic process involving sexual maturation and gaining ability of reproduction, is a complex trait in individual development. Onset of puberty ,the time of which is an key parameter in puberty, is triggered by reactivation of the hypothalamic-pituitary-gonadal （HPG） axis. Puberty is modulated by both genetic and environmental factors.Moreover, variation of this medically important trait can be also consequence of maternal effects, through various regulatory nodes such as cytoplasmic factors, intrauterine environment and etc. The inbred mouse strains C3H/HeJ（C3H） and C57BL/6J（B6） were used as model animals in this study, by transplantation of hybridized F1 zygotes B6C3HF1（B6♀x C3H♂） and C3HB6F1（C3H♀x B6♂） to the oviducts of these two strains. Then F1 zygotes can undergo development in the uterus. Finally,the zygotes from reciprocal crosses can be found in the uterus of C3H and B6. Genotyping of the two types of zygotes from reciprocal crosses were performed with SNP assay of mtDNA and therefore the origin of the zygotes can be identified. The age at VO, an phenotype to quantify pubertal timing of all female mice and age at BPS ,an phenotype to quantify pubertal timing of all male mice were recorded. Maternal effects were monitored though intensive phenotyping of the transplanted progeny. Comparative study were performed both between zygotes of the uniform genotypes from different uterus environment and between zygotes of different genotypes from the same uterus environment. To identify molecular factors for maternal effects, multiple molecular quantification at 10^th and 19^th day of pregnancy in female mice were performed including blood sugar, leptin and corticosteroids to address the intrauterine environmental factors that may be responsible for the pubertal timing.The study found that the puberty onset timing of BPS in F1 males not VO in females, which underwent development in different uterus environment, is significantly different. However, there were no differences in puberty onset timing between the two types zygotes from the identical uterus neither in males nor in females. It can be speculated that intrauterine environment is the major factors which impact the puberty onset timing in F1. And cytoplasmic factors were not observed significantly causative to pubertal events. The study also found that pubertal development as shown by BPS in the males were less affected in comparison to females in which significant of delayed puberty onset were observed when the zygotes underwent transplantation into uterus. When the comparison of moleculars in blood of pregnant mice was performed, significant discrepancies of the tested sugar level were found between the C3H and B6 strains at both of the phenotyping window specified above. It can be concludeded that sugar can impact the development of male F1 in the uters, and the impact the puberty onset timing after birth. As a type of nutrition sugar may influence the body weight and then affect the puberty. As the level of leptin change in different inbred strains at 19^th day of pregnancy were observed, there was significant evidence of its association with pubertal timing. And it may work on the development of male embryos in the late pregnancy in the uterus, then it can impact the puberty onset of F1 after birth. In addition, the corticosterones differ significantly between the two pregnant periods in C3H inbred strains, which can be considered a important hormonal factor that impacted the growth of the embryos. But it maybe not the crucial factors to the puberty onset of F1 progeny.