Spermatogenesis in mammals is crucial for male fertility. It starts after birth and continues throughout life, relying on spermatogonial stem cells (SSCs). SSCs can differentiate into early spermatogonia while maintaining their own pool. Early spermatogonia develop into mature spermatogonia through mitotic divisions, and type B spermatogonia further develop into mature sperm cells. This complex process is fundamental for male reproductive function. The centrosomal linker protein C-Nap1 is important in the centrosome. Its absence in non-transformed RPE1 cells leads to loss of centrosome linker activity. Recent studies show that C-Nap1 knockout male mice are infertile, but there are contradictions in phenotypes and the underlying molecular mechanisms of defective spermatogenesis remain unclear.

Recently, Quantitative Biology published an article entitled “Single-cell analyses reveal impaired type B spermatogonia differentiation and meiotic entry in C-Nap1-null testes”, which uses single-cell RNA sequencing to analyze wild-type and C-Nap1 knockout mouse testes to explore the role of C-Nap1 in spermatogenesis.

In this study, the impact of C-Nap1 on spermatogenesis using C-Nap1 knockout mouse models was investigated. Single-cell RNA sequencing of 10-day testes from wild-type and knockout mice was performed. Results showed that C-Nap1 deficiency led to male infertility, with reduced testicular spermatogonia and spermatocytes. Five spermatogonial stages were identified, and it was found that type B spermatogonia differentiation and meiotic initiation were impaired. Gene ontology enrichment analysis verified the downregulation of meiosis-specific genes. Some potentially affected genes like Ctnnb1 and Aurka were identified, indicating that C-Nap1 is essential for the mitosis-to-meiosis transition in spermatogonia.
DOI: 10.1002/qub2.71