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Mouse Tspyl5 promotes spermatogonia proliferation through enhancing Pcna-mediated DNA replication

Xiangyou Leng1, Shengyu Xie1, Dachang Tao1

  • 1Department of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.

Reproduction, Fertility, and Development
|January 7, 2024
PubMed
Abstract

Insights

Testis-specific protein Y-linked like 5 (TSPYL5) regulates spermatogenesis by maintaining spermatogonia proliferation and enhancing DNA replication. Tspyl5 deficiency in mice reduced fertility and sperm counts, highlighting its crucial role.

Area of Science:

  • Reproductive Biology
  • Molecular Genetics
  • Developmental Biology

Background:

  • The human TSPY1 gene is vital for spermatogenesis and male fertility.
  • Studying TSPY1 function is challenging due to a mouse pseudogene.
  • TSPYL5, a homologous gene, is expressed in testes and may influence spermatogenesis.

Purpose of the Study:

  • Investigate the role of Tspyl5 in spermatogenesis.
  • Understand the mechanism of Tspyl5 in male fertility.
  • Explore Tspyl5's relationship with TSPY1 function.

Main Methods:

  • Generated Tspyl5-knockout mice.
  • Analyzed spermatogenesis in knockout mice.
  • Performed transcriptomic analysis of spermatogonia.

Main Results:

  • Tspyl5 deficiency led to reduced fertility and lower spermatogonia/spermatozoa counts in aged mice.
  • Downregulation of the Pcna-mediated DNA replication pathway was observed in Tspyl5-knockout spermatogonia.
  • Tspyl5 promotes spermatogonia proliferation and Pcna expression via TRP53 ubiquitination-degradation.

Conclusions:

  • Tspyl5 positively regulates spermatogonia pool maintenance by enhancing Pcna-mediated DNA replication.
  • This study offers insights into the spermatogenesis-related functions of TSPY1.

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