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<p>In mouse early pachytene spermatocytes, the X and Y chromosomes undergo rapid non-homologous (NH) synapsis and desynapsis, but the functional significance remains unknown. Here, we report that pachynema-specific knockout of Speedy A (SpdyA) from telomeres caused persistent <i>Y-X NH synapsis</i>, with the entire Y axis synapsed onto the X axis. This persistent <i>Y-X NH synapsis</i> did not interrupt meiotic sex chromosome inactivation, recombination, or sex body formation, but it disrupted X-Y&#xa0;loop-axis organization and homologous X-Y desynapsis, leading to spermatocyte death. Similarly, persistent <i>Y-X NH synapsis</i> was also observed in pachytene spermatocytes lacking TRF1, where SpdyA was frequently lost from the&#xa0;X-Y non-pseudoautosomal region (non-PAR) telomeres. Mechanistic studies revealed that Serine 48 of SUN1 is a key SpdyA/CDK2 phosphorylation site required for Y-X NH desynapsis. We propose that SpdyA governs Y-X NH desynapsis by stabilizing the linkage between the X-Y non-PAR telomeres and their LINC complexes, and that this process is regulated independently from other aspects of pachynema progression. Our findings suggest a key role for Y-X NH desynapsis in establishing proper X-Y&#xa0;loop-axis organization.</p>

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Speedy A governs non-homologous XY chromosome desynapsis as a unique prerequisite for XY loop-axis organization

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月18日

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  • Dongteng Liu,
  • Yuxiang Zhang,
  • Dongliang Li,
  • Binjie Jiang,
  • Xudong Zhao,
  • Yanyan Li,
  • Zexiong Lin,
  • Yu Zhao,
  • Zhe Hu,
  • Shuzi Deng,
  • Zheng Li,
  • Haonan Lu,
  • Karen K L Chan,
  • William S B Yeung,
  • Philipp Kaldis,
  • Chencheng Yao,
  • Hengbin Wang,
  • Louise T Chow,
  • Kui Liu

摘要

In mouse early pachytene spermatocytes, the X and Y chromosomes undergo rapid non-homologous (NH) synapsis and desynapsis, but the functional significance remains unknown. Here, we report that pachynema-specific knockout of Speedy A (SpdyA) from telomeres caused persistent Y-X NH synapsis, with the entire Y axis synapsed onto the X axis. This persistent Y-X NH synapsis did not interrupt meiotic sex chromosome inactivation, recombination, or sex body formation, but it disrupted X-Y loop-axis organization and homologous X-Y desynapsis, leading to spermatocyte death. Similarly, persistent Y-X NH synapsis was also observed in pachytene spermatocytes lacking TRF1, where SpdyA was frequently lost from the X-Y non-pseudoautosomal region (non-PAR) telomeres. Mechanistic studies revealed that Serine 48 of SUN1 is a key SpdyA/CDK2 phosphorylation site required for Y-X NH desynapsis. We propose that SpdyA governs Y-X NH desynapsis by stabilizing the linkage between the X-Y non-PAR telomeres and their LINC complexes, and that this process is regulated independently from other aspects of pachynema progression. Our findings suggest a key role for Y-X NH desynapsis in establishing proper X-Y loop-axis organization.