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<p>Transposable elements (TEs) in the human genome are the heritage of ancient parasitic infections. While most of human DNA comprises TEs and TE-derived elements, their repetitive nature poses technical challenges; thus, little is known about their positional identity and regulatory roles. Here, by integrating long-read and multidimensional transcriptional analyses, we investigate when, where and how TEs become part of a gene. We characterize how TE-derived isoforms change across mouse–human variation and how they are linked to gene regulatory networks controlling cell states during differentiation, organogenesis and health (aging and pathological states). Mechanistically, we identify an RNA degradation-dependent and splicing-dependent quality control mechanism that operates independently of conventional mechanisms of TE suppression, such as DNA methylation and heterochromatinization, and prevents TE-chimera expression and TE-induced cell differentiation. Overall, our findings unveil mechanisms by which viral-derived elements enhance transcriptome plasticity.</p>

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Transposable element–gene chimera cartography, origination and role in enhancing transcriptome plasticity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月25日

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  • Youngseo Cheon,
  • Erik Glen Alvstad,
  • Denis Torre,
  • Daniel Tu Quach,
  • Jennifer Nguyen,
  • Kwangbeom Hyun,
  • Mingqi Zhou,
  • Tianxiong Yu,
  • Liang Liu,
  • Yoseop Yoon,
  • Fairlie Reese,
  • Lauren Faraone,
  • Yingcong Li,
  • Frederick J. Arnold,
  • Yesai S. Fstkchyan,
  • Uttiya Basu,
  • Evgeny Kvon,
  • Enza Maria Valente,
  • Jessica Sook Yuin Ho,
  • Minji Byun,
  • Ernesto Guccione,
  • Yongsheng Shi,
  • Zhiping Weng,
  • Marcus Seldin,
  • Ivan Marazzi

摘要

Transposable elements (TEs) in the human genome are the heritage of ancient parasitic infections. While most of human DNA comprises TEs and TE-derived elements, their repetitive nature poses technical challenges; thus, little is known about their positional identity and regulatory roles. Here, by integrating long-read and multidimensional transcriptional analyses, we investigate when, where and how TEs become part of a gene. We characterize how TE-derived isoforms change across mouse–human variation and how they are linked to gene regulatory networks controlling cell states during differentiation, organogenesis and health (aging and pathological states). Mechanistically, we identify an RNA degradation-dependent and splicing-dependent quality control mechanism that operates independently of conventional mechanisms of TE suppression, such as DNA methylation and heterochromatinization, and prevents TE-chimera expression and TE-induced cell differentiation. Overall, our findings unveil mechanisms by which viral-derived elements enhance transcriptome plasticity.