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<p>METTL3 is a crucial mRNA methyltransferase in mammals, essential for the regulation of gene expression and various biological processes. Here, we demonstrate that <i>Mettl3</i> knockout (KO) in mouse embryonic stem cells (mESCs) leads to widespread upregulation of transposable elements (TEs) and 2-cell (2C)-like genes in a m<sup>6</sup>A enzyme activity-dependent manner, independent of culture conditions. Furthermore, embryo chimera experiments using a transient METTL3 degradation system (dTAG) revealed that METTL3-deficient mESCs can contribute to trophectoderm lineages at the blastocyst stage, indicative of expanded developmental potential. These findings highlight the role of METTL3-mediated m<sup>6</sup>A modifications in regulating the transcriptional and developmental plasticity of mESCs and suggest a link between m<sup>6</sup>A loss and the acquisition of a 2C-like state with features of extended potency.</p>

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The role of METTL3 in transposable elements regulation and 2C-like program induction in mouse embryonic stem cell

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月20日

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  • Xiuyu Chen,
  • Bingqiu Chen,
  • Yingying Zhao,
  • Ziyi Wen,
  • Jiajie Hao,
  • Lingmei Jin,
  • Danfeng Li,
  • Xiongzhi Quan,
  • Kaixin Wu,
  • Mingqiang Deng,
  • Xichen Bao,
  • Jie Wang,
  • Jiekai Chen

摘要

METTL3 is a crucial mRNA methyltransferase in mammals, essential for the regulation of gene expression and various biological processes. Here, we demonstrate that Mettl3 knockout (KO) in mouse embryonic stem cells (mESCs) leads to widespread upregulation of transposable elements (TEs) and 2-cell (2C)-like genes in a m6A enzyme activity-dependent manner, independent of culture conditions. Furthermore, embryo chimera experiments using a transient METTL3 degradation system (dTAG) revealed that METTL3-deficient mESCs can contribute to trophectoderm lineages at the blastocyst stage, indicative of expanded developmental potential. These findings highlight the role of METTL3-mediated m6A modifications in regulating the transcriptional and developmental plasticity of mESCs and suggest a link between m6A loss and the acquisition of a 2C-like state with features of extended potency.