Effect of deletion of ubiquitin carboxyl-terminal hydrolase 1 gene on the development of female mouse reproductive system

  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 deletion lose weight, have difficulty in exercising, and become 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 much smaller than heterozygous mice. There are some primitive or closed follicles in the ovarian cortex, but no mature follicles. And corpus luteum. UCHL1 lacks estrogen receptor (ER), follicle stimulating hormone receptor (luteinizing hormone receptor, LHR), luteinizing hormone receptor (LHR), progesterone receptor (PR) and other major reproductive receptors│ Ovarian ER The expression level in the ovaries of homozygous and heterozygous mice and homozygous mice was 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.