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<p><i>N</i><sup>1</sup>-methyladenosine (m<sup>1</sup>A) is a recently identified mRNA methylation mark that affects gene expression and translation. In the model plant <i>Arabidopsis thaliana</i>, its landscape and function remain uncharacterized. Here we present base-resolution m<sup>1</sup>A methylomes across diverse <i>Arabidopsis</i> tissues and show that m<sup>1</sup>A is enriched in the 5′ untranslated region and preferentially localizes to highly expressed genes, negatively correlating with mRNA translation. We demonstrate that TRM6 and TRM61 form the m<sup>1</sup>A methyltransferase complex and interact with ATH3 to regulate m<sup>1</sup>A levels. Notably, we identify previously unknown m<sup>1</sup>A readers, including CP33B and ECT2. Functional analyses reveal that m<sup>1</sup>A is intricately involved in abscisic acid (ABA) signalling and that knockout or knockdown of key genes in m<sup>1</sup>A RNA methylation causes ABA hypersensitivity. Collectively, our findings establish m<sup>1</sup>A as a dynamic epitranscriptomic mark, highlighting its critical role in regulating the ABA signalling pathway.</p>

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N1-methyladenosine mRNA methylation in Arabidopsis

  • 期刊论文

  • 发表日期：

    2026年7月17日

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  • Yunzhuo Ke,
  • Huanwei Huang,
  • Zhi-Yang Hou,
  • Mengjiao Zhang,
  • Xuemin Zhang,
  • Yao Qin,
  • Linxia Li,
  • Yixin Wang,
  • Cuiling Miao,
  • Zexuan Wu,
  • Changmei Hua,
  • Lisha Shen,
  • Hao Yu,
  • Zhe Liang

摘要

N1-methyladenosine (m1A) is a recently identified mRNA methylation mark that affects gene expression and translation. In the model plant Arabidopsis thaliana, its landscape and function remain uncharacterized. Here we present base-resolution m1A methylomes across diverse Arabidopsis tissues and show that m1A is enriched in the 5′ untranslated region and preferentially localizes to highly expressed genes, negatively correlating with mRNA translation. We demonstrate that TRM6 and TRM61 form the m1A methyltransferase complex and interact with ATH3 to regulate m1A levels. Notably, we identify previously unknown m1A readers, including CP33B and ECT2. Functional analyses reveal that m1A is intricately involved in abscisic acid (ABA) signalling and that knockout or knockdown of key genes in m1A RNA methylation causes ABA hypersensitivity. Collectively, our findings establish m1A as a dynamic epitranscriptomic mark, highlighting its critical role in regulating the ABA signalling pathway.