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<p>The endoplasmic reticulum (ER) mitigates stress typically through unfolded protein response (UPR) and ER-associated degradation (ERAD) pathways, yet post-transcriptional regulation of ER stress remains poorly defined. <i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) modification, predominantly enriched near stop codons, can govern mRNA fates via P-bodies or stress granules in stress conditions. m<sup>6</sup>A also occurs within coding sequences (CDS–m<sup>6</sup>A), but its role remains unappreciated in plants. Here we demonstrate that m<sup>6</sup>A ablation sensitizes <i>Arabidopsis</i> ER stress despite normal UPR and ERAD activities. Mechanistically, CDS–m<sup>6</sup>A co-localizes with ribosome stalling sites and directs co-translational RNA decay (CTRD). Under stress, activation of m<sup>6</sup>A-triggered CTRD accelerates clearance of ER-engaged transcripts, thereby alleviating translational overload. During geminivirus infection, which increases translational demand on ER, m<sup>6</sup>A-triggered CTRD also targets viral RNAs, restricting their accumulation, translation and disease progression. Thus, CDS–m<sup>6</sup>A functions as a pivotal regulator of ER-linked RNA surveillance, establishing an organelle-specific mechanism that integrates RNA stability, protein homeostasis and antiviral defence.</p>

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CDS-localized m6A drives co-translational RNA decay to relieve biotic and abiotic endoplasmic reticulum stresses

  • 期刊论文

  • 发表日期：

    2026年5月8日

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  • Songxiao Zhong,
  • Tae Rin Oh,
  • Xindi Li,
  • Jinming Zhang,
  • Suk Won Choi,
  • Chuyun Gao,
  • Xu Peng,
  • Juan Dong,
  • Chuan He,
  • Xiuren Zhang

摘要

The endoplasmic reticulum (ER) mitigates stress typically through unfolded protein response (UPR) and ER-associated degradation (ERAD) pathways, yet post-transcriptional regulation of ER stress remains poorly defined. N6-methyladenosine (m6A) modification, predominantly enriched near stop codons, can govern mRNA fates via P-bodies or stress granules in stress conditions. m6A also occurs within coding sequences (CDS–m6A), but its role remains unappreciated in plants. Here we demonstrate that m6A ablation sensitizes Arabidopsis ER stress despite normal UPR and ERAD activities. Mechanistically, CDS–m6A co-localizes with ribosome stalling sites and directs co-translational RNA decay (CTRD). Under stress, activation of m6A-triggered CTRD accelerates clearance of ER-engaged transcripts, thereby alleviating translational overload. During geminivirus infection, which increases translational demand on ER, m6A-triggered CTRD also targets viral RNAs, restricting their accumulation, translation and disease progression. Thus, CDS–m6A functions as a pivotal regulator of ER-linked RNA surveillance, establishing an organelle-specific mechanism that integrates RNA stability, protein homeostasis and antiviral defence.