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<p>In mammals, X-linked dosage compensation involves X-chromosome inactivation to balance X chromosome dosage between males and females, and hyperactivation of the remaining X-chromosome (Xa-hyperactivation) to achieve X-autosome balance in both sexes. Studies of both processes have largely focused on coding genes and have not accounted for transposable elements which comprise 50% of the X-chromosome with numerous epigenetic functions. Here we develop a new bioinformatic pipeline tailored to repetitive elements with capability for allelic discrimination. We then apply the pipeline to our recent So-Smart-Seq analysis of single embryos to comprehensively interrogate whether X-linked transposable elements are subject to either X-chromosome inactivation or Xa-hyperactivation. We observe significant differences in repeat silencing in parentally driven “imprinted” versus zygotically driven “random” X-chromosome inactivation. Chromosomal positioning, genetic background and evolutionary age impact their silencing. In contrast, transposable elements do not undergo Xa-hyperactivation. Evolutionary and functional implications are discussed.</p>

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Dynamic dosage changes in X-linked transposable elements during mammalian dosage compensation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月11日

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  • Chunyao Wei,
  • Barry Kesner,
  • Uri Weissbein,
  • Peera Wasserzug-Pash,
  • Priyojit Das,
  • Jeannie T. Lee

摘要

In mammals, X-linked dosage compensation involves X-chromosome inactivation to balance X chromosome dosage between males and females, and hyperactivation of the remaining X-chromosome (Xa-hyperactivation) to achieve X-autosome balance in both sexes. Studies of both processes have largely focused on coding genes and have not accounted for transposable elements which comprise 50% of the X-chromosome with numerous epigenetic functions. Here we develop a new bioinformatic pipeline tailored to repetitive elements with capability for allelic discrimination. We then apply the pipeline to our recent So-Smart-Seq analysis of single embryos to comprehensively interrogate whether X-linked transposable elements are subject to either X-chromosome inactivation or Xa-hyperactivation. We observe significant differences in repeat silencing in parentally driven “imprinted” versus zygotically driven “random” X-chromosome inactivation. Chromosomal positioning, genetic background and evolutionary age impact their silencing. In contrast, transposable elements do not undergo Xa-hyperactivation. Evolutionary and functional implications are discussed.