BACKGROUND: Male infertility is a major issue in human reproduction health, yet known genetic factors are only responsible for a small fraction of cases. TSGA10 is a testis-specific protein that is highly conserved among different species. A previous study has reported a homozygous mutation in TSGA10 in a male infertile patient; however, function analysis of Tsga10 genes in knockout mice has not yet been undertaken. OBJECTIVES: The aim of the present work was to analyse the function of TSGA10 protein in the spermatogenesis of Tsga10+/- mice. MATERIALS AND METHODS: Tsga10+/- mice were generated by CRISPR/Cas9 technology, in vitro fertilization (IVF), western blot, co-immunoprecipitation and other methods were used to the function analysis. RESULTS: Heterozygous Tsga10 male mice created by CRISPR/Cas9 were infertile and presented significantly reduced sperm motility because of disordered mitochondrial sheath formation. Furthermore, TSGA10 can interact with GRP78 and NSUN2, which are associated with peri-implantation lethality and the gonadotropin-releasing hormone (GnRH) network. DISCUSSION AND CONCLUSION: We demonstrate that deficiency of Tsga10 gene can lead to male infertility in mice. TSGA10 is involved in the correct arrangement of mitochondrial sheath in spermatozoa. Future studies on TSGA10 include an in-depth exploration of the underlying mechanisms of TSGA10 in spermatogenesis, early embryonic development and GnRH network.
BACKGROUND:Male infertility is a major issue in human reproduction health, yet known genetic factors are only responsible for a small fraction of cases. TSGA10 is a testis-specific protein that is highly conserved among different species. A previous study has reported a homozygous mutation in TSGA10 in a male infertilepatient; however, function analysis of Tsga10 genes in knockout mice has not yet been undertaken. OBJECTIVES: The aim of the present work was to analyse the function of TSGA10 protein in the spermatogenesis of Tsga10+/- mice. MATERIALS AND METHODS:Tsga10+/- mice were generated by CRISPR/Cas9 technology, in vitro fertilization (IVF), western blot, co-immunoprecipitation and other methods were used to the function analysis. RESULTS: Heterozygous Tsga10 male mice created by CRISPR/Cas9 were infertile and presented significantly reduced sperm motility because of disordered mitochondrial sheath formation. Furthermore, TSGA10 can interact with GRP78 and NSUN2, which are associated with peri-implantation lethality and the gonadotropin-releasing hormone (GnRH) network. DISCUSSION AND CONCLUSION: We demonstrate that deficiency of Tsga10 gene can lead to male infertility in mice. TSGA10 is involved in the correct arrangement of mitochondrial sheath in spermatozoa. Future studies on TSGA10 include an in-depth exploration of the underlying mechanisms of TSGA10 in spermatogenesis, early embryonic development and GnRH network.