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METTL5介导的18S rRNA mA修饰增强了核糖体组装及脱落酸应答。 (原文中“in”后面缺少具体内容)

METTL5-mediated 18S rRNA mA modification enhances ribosome assembly and ABA response in .

作者信息

Li Ping, Zhang Yu, Zhang Songyao, Ma Jinqi, Fan Sheng, Shen Lisha

机构信息

Temasek Life Sciences Laboratory National University of Singapore Singapore Singapore.

Department of Biological Sciences National University of Singapore Singapore Singapore.

出版信息

Imeta. 2025 Jun 13;4(4):e70055. doi: 10.1002/imt2.70055. eCollection 2025 Aug.

Abstract

METTL5 catalyzes the -methyladenosine (mA) methylation at A in 18S rRNA, a modification essential for its association with the ribosomal protein RPL24A, facilitating the assembly of 80S ribosome. This facilitates the translation of mRNAs encoding the detoxifying glutathione S-transferase (GST) enzymes, thereby maintaining normal reactive oxygen species (ROS) levels and ensuring proper abscisic acid (ABA) responses. In mutants, the absence of mA compromises RPL24A incorporation and ribosome assembly, impairing the translation of GSTs. This results in ROS excessive accumulation and hypersensitivity to ABA.

摘要

METTL5催化18S核糖体RNA中A位点的N6-甲基腺苷(mA)甲基化,这种修饰对于其与核糖体蛋白RPL24A的结合至关重要,有助于80S核糖体的组装。这促进了编码解毒谷胱甘肽S-转移酶(GST)酶的mRNA的翻译,从而维持正常的活性氧(ROS)水平并确保适当的脱落酸(ABA)反应。在突变体中,mA的缺失会损害RPL24A的掺入和核糖体组装,从而损害GST的翻译。这导致ROS过度积累和对ABA的超敏反应。

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