动物造模,基因敲除 z-bio 2022-04-16 603

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

　　Methods: CRISPR/Cas9 technology was used to obtain Fancm knockout mice. The expression of FANCM protein in the testis tissue of wild-type and Fancm-/- mice was analyzed. The reproductive status of the offspring was analyzed, and the blood routine indexes were analyzed.

　　Results: The ATG region of Fancm gene was knocked out to obtain Fancm-/- mice with stable inheritance of C57BL/6 background. The expression of FANCM protein 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 was significantly less than that of male Fancm-/- mice. There was no significant difference in wild-type body weight between the littermates of Fancm-/- mice, and some blood routine indexes were significantly different. Fancm-/- Mice have obvious reproductive defects. Male Fancm-/- mice have significant developmental defects in the testis, increased spermatogenic cell apoptosis and cell cycle arrest, which affect testicular development and spermatogenesis.

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