Centromere protein CEP170 is dispensable for mouse spermatogenesis and male fertility.

Spermatogenesis is crucial for male fertility and involves highly coordinated cellular differentiation, which depends on mitosis, meiosis, and cellular transformation processes that all require dynamic remodeling of the microtubule cytoskeleton. Microtubule anchoring, spindle assembly, and ciliary control all depend on centromere protein 170 (CEP170), which is found in the subdistal pole of the centrosome. CEP170 is regarded as a promising option for controlling male fertility because of its high expression in the testes and interactions with meiotic proteins. Given the embryonic lethality associated with complete CEP170 knockout, we generated germline-specific Cep170 knockout (KO) mice using CRISPR/Cas9 technology to investigate its role in male fertility. Surprisingly, our results show that Cep170 KO males remain fertile, producing litter sizes comparable to those of wild-type (WT) controls. Testis weight and histological architecture were unaffected. Computer-assisted sperm analysis (CASA) revealed no significant differences in sperm motility, concentration, or morphology between KO and WT mice. Moreover, detailed analysis of testicular sections using stage-specific markers for spermatogonia, spermatocytes, and spermatids showed no disruptions in germ cell proliferation, meiotic progression, or spermatogenesis. These findings indicate that, despite its high expression in the testis and established cellular functions, CEP170 is not essential for spermatogenesis or male fertility in mice. This study further refines the molecular network governing male fertility, particularly with respect to centrosome-associated proteins.