Loss of TEX30 leads to male subfertility in mice.

Tex30, a member of the "testis-expressed" genes, has been implicated in spermatogenesis due to its high expression in the testes, localized in both the cytoplasmic and soluble nuclear fractions of testicular cells. However, its precise role in germ cell development remains unclear. In this study, we generated Tex30 knockout (KO) mice by utilizing the CRISPR/Cas9-mediated gene KO approach and comprehensively investigated its function in reproduction. The results revealed that the male Tex30 KO mice exhibited increased apoptosis in metaphase I spermatocytes, premature dissociation of XY chromosomes in late spermatocytes, and spermiogenic defects, leading to a significant reduction in sperm production and motility, and thus final subfertility. The adult female Tex30 KO mice did not show significant differences in ovaries and fertility when compared with the control females. IP-MS-based identification of TEX30 interactomes in testis unveils its role in RNA metabolism and cytoskeletal regulation, whose dysregulation resulted from TEX30 ablation may account for the reproductive phenotype in male mice. Taken together, the data presented in this study suggest that TEX30 plays a role in spermatogenesis and male fertility.