The biological functions of the epitranscriptomic modification N⁶-methyladenosine (m⁶A) in plants are not fully understood. CPSF30-L is a predominant isoform of the polyadenylation factor CPSF30 and consists of CPSF30-S and an m⁶A-binding YTH domain. Little is known about the biological roles of CPSF30-L and the molecular mechanism underlying its m⁶A-binding function in alternative polyadenylation. Here, we characterized CPSF30-L as an Arabidopsis m⁶A reader whose m⁶A-binding function is required for the floral transition and abscisic acid (ABA) response. We found that the m⁶A-binding activity of CPSF30-L enhances the formation of liquid-like nuclear bodies, where CPSF30-L mainly recognizes m⁶A-modified far-upstream elements to control polyadenylation site choice. Deficiency of CPSF30-L lengthens the 3′ untranslated region of three phenotypes-related transcripts, thereby accelerating their mRNA degradation and leading to late flowering and ABA hypersensitivity. Collectively, this study uncovers a new molecular mechanism for m⁶A-driven phase separation and polyadenylation in plants.

尚未完全了解植物中表观转录组修饰N ⁶ -甲基腺苷(m ⁶ A)的生物学功能。CPSF30-L 是聚腺苷酸化因子 CPSF30 的主要同种型，由 CPSF30-S 和 m ⁶ A 结合 YTH 结构域组成。关于 CPSF30-L 的生物学作用及其在替代聚腺苷酸化中的m ⁶ A 结合功能的分子机制知之甚少。在这里，我们将 CPSF30-L 表征为拟南芥m ⁶ A 阅读器，其 m ⁶ A 结合功能是花转化和脱落酸 (ABA) 响应所必需的。我们发现 m ⁶CPSF30-L 的 A 结合活性增强了液体样核体的形成，其中 CPSF30-L 主要识别 m ⁶ A 修饰的远上游元件以控制聚腺苷酸化位点的选择。CPSF30-L 的缺乏会延长三种表型相关转录物的 3' 非翻译区，从而加速它们的 mRNA 降解并导致晚花和 ABA 超敏反应。总的来说，这项研究揭示了植物中m ⁶ A 驱动的相分离和聚腺苷酸化的新分子机制。