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拟南芥 N6-甲基腺苷阅读蛋白 CPSF30-L 识别 FUE 信号,以控制液滴状核体内的多聚腺苷酸化位点选择。

Arabidopsis N-methyladenosine reader CPSF30-L recognizes FUE signals to control polyadenylation site choice in liquid-like nuclear bodies.

机构信息

Synthetic and Functional Biomolecules Center, Beijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, College of Chemistry and Molecular Engineering, Peking University, Beijing 100871, China.

Medical Isotopes Research Center and, Department of Radiation Medicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.

出版信息

Mol Plant. 2021 Apr 5;14(4):571-587. doi: 10.1016/j.molp.2021.01.014. Epub 2021 Jan 27.

Abstract

The biological functions of the epitranscriptomic modification N-methyladenosine (mA) in plants are not fully understood. CPSF30-L is a predominant isoform of the polyadenylation factor CPSF30 and consists of CPSF30-S and an mA-binding YTH domain. Little is known about the biological roles of CPSF30-L and the molecular mechanism underlying its mA-binding function in alternative polyadenylation. Here, we characterized CPSF30-L as an Arabidopsis mA reader whose mA-binding function is required for the floral transition and abscisic acid (ABA) response. We found that the mA-binding activity of CPSF30-L enhances the formation of liquid-like nuclear bodies, where CPSF30-L mainly recognizes mA-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 mA-driven phase separation and polyadenylation in plants.

摘要

N6-甲基腺苷(m6A)作为一种转录后修饰,其在植物中的生物学功能尚未完全阐明。多聚腺苷酸化因子 CPSF30 的主要亚型是 CPSF30-L,它由 CPSF30-S 和一个 m6A 结合的 YTH 结构域组成。关于 CPSF30-L 的生物学功能及其在可变多聚腺苷酸化中 m6A 结合功能的分子机制知之甚少。在这里,我们将 CPSF30-L 鉴定为一种拟南芥 m6A 阅读器,其 m6A 结合功能对于花发育和脱落酸(ABA)反应是必需的。我们发现 CPSF30-L 的 m6A 结合活性增强了液-液相分离核体的形成,其中 CPSF30-L 主要识别 m6A 修饰的上游元件,以控制多聚腺苷酸化位点选择。CPSF30-L 的缺失会使三个与表型相关的转录本的 3'非翻译区延长,从而加速它们的 mRNA 降解,导致开花延迟和 ABA 超敏反应。总之,这项研究揭示了 m6A 驱动的植物相分离和多聚腺苷酸化的新分子机制。

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