
Problem statement: our understanding of male meiosis and male infertility at the molecular level is incomplete.
Methods: a transgenic mouse model with conditional knockout of Pax transactivation domain-interacting protein (PTIP) in postnatal male germ cells has been generated and utilized for reproduction phenotyping and molecular and cellular analyses.
Results: our data demonstrate that PTIP deficiency in male germ cells leads to spermatogenesis arrest in meiosis prophase I, defective DNA damage repair, azoospermia, and sterility.
Conclusion: PTIP plays an essential role in male meiosis. This finding may hold clinical relevance in human reproduction.