动物造模,基因敲除 z-bio 2021-11-12 260

　　Aim: To construct Fancm gene knockout mice of Fanconi anemia pathway and study the effect of Fancm gene deletion on the physiological functions of mice, especially the male reproductive organs.

　　Methods: Using CRISPR/Cas9 technology to obtain Fancm gene knockout mice. Analyze the expression of FANCM protein in wild-type and Fancm-/- mouse testis. Count the birth rate, weight, sex ratio of Fancm-/- mice and The fertility status of the offspring, and the routine blood indicators were analyzed. Histomorphological study of the physiological and pathological phenotypes of the testes of male Fancm-/- mice.

　　Results: Knock out the ATG region of the Fancm gene to obtain a stable inherited C57BL/6 background Fancm-/- mouse. The FANCM protein expression in the testis of Fancm-/- mice was completely lost. There was no obvious embryonic lethality in Fancm-/- mice , But the number of female Fancm-/- mice is significantly less than that of male Fancm-/- mice. There is no significant difference in body weight compared with wild-type Fancm-/- mice in the same litter, and there are significant differences in some blood routine indicators. Fancm-/- Mice have obvious reproductive capacity defects. Male Fancm-/- mice have significant developmental defects in their testes, with increased spermatogenic cell apoptosis and cell cycle arrest, which affects testicular development and sperm production.

　　Conclusion: Successfully obtained stable genetic C57BL/6 background Fancm-/- mice, Fancm gene is involved in the growth and development of mice, especially the maintenance and regulation of the function of male reproductive organs.