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<p>Tuberculosis (TB), the leading cause of death from a single infectious agent, remains incompletely understood in its pathogenic mechanisms. Through population-based bioinformatic analyses, we identified m<sup>6</sup>A modifications may play a critical role in the infection dynamics of tuberculosis, with CAPRIN1 emerging as a TB-specific m<sup>6</sup>A regulatory factor. Molecular and cellular experiments demonstrated that CAPRIN1 regulates the m<sup>6</sup>A modification of RIG-I RNA through direct interaction with METTL3, further influencing downstream interferon-associated gene networks and modulating <i>Mycobacterium tuberculosis</i> (<i>M. tuberculosis</i>) infection. Moreover, we discovered that these molecular biological processes predominantly occur within cellular stress granules (SGs). In summary, this study elucidates a CAPRIN1-specific m<sup>6</sup>A modification mechanism targeting RIG-I, proposing a potential target for the prevention and treatment of TB. and contributing to the theory of m<sup>6</sup>A’s specific regulatory roles.</p>

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CAPRIN1 specifically mediates m6A modification of RIG-I RNA to inhibit Mycobacterium Tuberculosis infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月6日

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  • Lijuan Zhou,
  • Hubin Chen,
  • Dan Jiang,
  • Xinyue Xu,
  • Zheng Li,
  • Ruili Zheng,
  • Jun Huang,
  • Yi Ling,
  • Yanyan Liao,
  • Hailong Wang,
  • Peijiang Pan,
  • Junjun Jiang,
  • Li Ye,
  • Wan Shuan Lee,
  • Yafei Chen,
  • Shiou Yih Lee,
  • Xiaoping Lv,
  • Jiemei Chu,
  • Hao Liang,
  • Sanqi An

摘要

Tuberculosis (TB), the leading cause of death from a single infectious agent, remains incompletely understood in its pathogenic mechanisms. Through population-based bioinformatic analyses, we identified m6A modifications may play a critical role in the infection dynamics of tuberculosis, with CAPRIN1 emerging as a TB-specific m6A regulatory factor. Molecular and cellular experiments demonstrated that CAPRIN1 regulates the m6A modification of RIG-I RNA through direct interaction with METTL3, further influencing downstream interferon-associated gene networks and modulating Mycobacterium tuberculosis (M. tuberculosis) infection. Moreover, we discovered that these molecular biological processes predominantly occur within cellular stress granules (SGs). In summary, this study elucidates a CAPRIN1-specific m6A modification mechanism targeting RIG-I, proposing a potential target for the prevention and treatment of TB. and contributing to the theory of m6A’s specific regulatory roles.