动物造模 z-bio 2021-09-29 318

　　OBJECTIVE: To study the effect of ubiquitin C-terminal hydrolase L1UCH-L1 gene deletion on the reproductive system of female mice.

　　Method: Use vaginal smear, immunohistochemistry, Western blotting, RNA interference to analyze the effect of UCH-L1 gene deletion on mouse ovarian function and follicular development.

　　Result: Adult female mice homozygous for the UCH-L1 gene defect lost weight, had difficulty exercising, and became thinner in the uterus. UCH-L1 protein expression cannot be detected in the ovaries and uterus of homozygous mice lacking UCH-L1 gene. The ovaries are significantly smaller than heterozygous mice, and some primitive or closed follicles are missing in the ovarian cortex. Mature follicles and uterus.. The main propagules, such as estrogen receptor (ER), follicle stimulating hormone receptor (luteinizing hormone receptor, LHR), luteinizing hormone receptor (LHR), progesterone receptor ( PR) receptor does not exist in UCHL1│ Homozygous and homozygous heterozygous mice are expressed in the ovary, and the ER expression level in the ovary of homozygous mice is significantly lower than that in heterozygous mice. Using NA interference to down-regulate the expression of UCH-LI in embryonic (GV) oocytes can significantly reduce the maturation rate of oocytes.

　　Conclusion: Female mice lacking the UCH-L1 gene cannot form mature follicles and ovulate, resulting in a significant decrease in ER expression in the ovary. It is speculated that UCH-L1 may affect the maturation and ovulation process of oocytes by down-regulating the expression of ER in the ovary.