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<p>Sexual dimorphism (SDM) is regulated by sex chromosomes, yet the specific contribution of individual genes remains unclear. To address this, we conducted a comprehensive phenotyping analysis to investigate the roles of Y chromosome-linked genes in SDM formation in mice. Using C57BL/6J mice, we identified 49 SDM traits across 14 biological systems. To assess gene-specific effects, we generated knockout (KO) mice for 10 unique Y-linked genes using CRISPR/Cas9. As expected, <i>Sry</i> KO resulted in feminization of most SDM traits, including gonadal sex. However, certain body size-related traits remained male-like, suggesting the involvement of additional Y-linked genes. Consistently, KOs of <i>Uty</i> and <i>Usp9y</i> significantly altered traits related to body and organ size. We further applied a dimensionality reduction approach to quantitatively capture SDM variation at the individual level, enabling visualization of phenotypic shifts in each KO mouse. Our findings demonstrate that non-<i>Sry</i> Y-linked genes contribute to SDM and introduce a generalizable framework for quantifying sex differences across individuals and species.</p>

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Quantitative dissection of sexual dimorphism in mice through Y-linked gene knockouts and multivariate phenotyping

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月6日

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  • Nobuhiko Tanaka,
  • Kento Miura,
  • Ai Ozaki,
  • Yasuyo Kozawa,
  • Masaru Tamura,
  • Atsuo Ogura,
  • Shogo Matoba

摘要

Sexual dimorphism (SDM) is regulated by sex chromosomes, yet the specific contribution of individual genes remains unclear. To address this, we conducted a comprehensive phenotyping analysis to investigate the roles of Y chromosome-linked genes in SDM formation in mice. Using C57BL/6J mice, we identified 49 SDM traits across 14 biological systems. To assess gene-specific effects, we generated knockout (KO) mice for 10 unique Y-linked genes using CRISPR/Cas9. As expected, Sry KO resulted in feminization of most SDM traits, including gonadal sex. However, certain body size-related traits remained male-like, suggesting the involvement of additional Y-linked genes. Consistently, KOs of Uty and Usp9y significantly altered traits related to body and organ size. We further applied a dimensionality reduction approach to quantitatively capture SDM variation at the individual level, enabling visualization of phenotypic shifts in each KO mouse. Our findings demonstrate that non-Sry Y-linked genes contribute to SDM and introduce a generalizable framework for quantifying sex differences across individuals and species.