MicroRNA-202 safeguards meiotic progression bypreventing premature SEPARASE-mediated REC8 cleavage

Jian Chen1,2,3, Chenxu Gao1,2,3,4, Mengcheng Luo5

  • 1State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

EMBO Reports
|June 17, 2022
PubMed

Insights

MicroRNA-202 (miR-202) is crucial for male fertility. Loss of miR-202 in mice disrupts meiosis, causing spermatocyte death and impacting sperm development.

Area of Science:

  • Reproductive Biology
  • Molecular Genetics
  • Cell Biology

Background:

  • MicroRNAs (miRNAs) are key regulators in mammalian spermatogenesis.
  • The specific in vivo functions of individual miRNAs during spermatogenesis are not fully understood.

Purpose of the Study:

  • To investigate the role of miR-202 in mammalian spermatogenesis.
  • To elucidate the molecular mechanisms underlying miR-202's function in meiosis.

Main Methods:

  • Phenotypic evaluation of miR-202 knockout (KO) mice.
  • Analysis of spermatocyte apoptosis and meiotic progression.
  • Identification of direct miRNA targets and downstream regulatory pathways.

Main Results:

  • miR-202 deficiency leads to spermatocyte apoptosis and disrupts the zygonema-to-pachynema transition.
  • Meiosis prophase I events, including synapsis and crossover formation, are impaired in miR-202 KO mice.
  • Separase mRNA is a direct target of miR-202, and miR-202 upregulates REC8 by repressing Separase.

Conclusions:

  • miR-202 is essential for normal spermatogenesis and male fertility.
  • miR-202 regulates meiosis by targeting the SEPARASE-REC8 axis.
  • This study identifies miR-202 as a novel noncoding gene regulator in meiotic processes.

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