Spliceosomal protein U2B″ delays leaf senescence by enhancing splicing variant JAZ9β expression to attenuate jasmonate signaling in Arabidopsis

IF 9.4 1区 生物学 Q1 Agricultural and Biological Sciences
New Phytologist Pub Date : 2023-08-22 DOI:10.1111/nph.19198
Qi Yang, Shuya Tan, Hou-Ling Wang, Ting Wang, Jie Cao, Hairong Liu, Yueqi Sha, Yaning Zhao, Xinli Xia, Hongwei Guo, Zhonghai Li
{"title":"Spliceosomal protein U2B″ delays leaf senescence by enhancing splicing variant JAZ9β expression to attenuate jasmonate signaling in Arabidopsis","authors":"Qi Yang,&nbsp;Shuya Tan,&nbsp;Hou-Ling Wang,&nbsp;Ting Wang,&nbsp;Jie Cao,&nbsp;Hairong Liu,&nbsp;Yueqi Sha,&nbsp;Yaning Zhao,&nbsp;Xinli Xia,&nbsp;Hongwei Guo,&nbsp;Zhonghai Li","doi":"10.1111/nph.19198","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>\n \n </p><ul>\n \n \n <li>\n \n <p>The regulatory framework of leaf senescence is gradually becoming clearer; however, the fine regulation of this process remains largely unknown.</p>\n </li>\n \n \n <li>\n \n <p>Here, genetic analysis revealed that U2 small nuclear ribonucleoprotein B (U2B″), a component of the spliceosome, is a negative regulator of leaf senescence. Mutation of U2B″ led to precocious leaf senescence, whereas overexpression of <i>U2B″</i> extended leaf longevity. Transcriptome analysis revealed that the jasmonic acid (JA) signaling pathway was activated in the <i>u2b″</i> mutant. U2B″ enhances the generation of splicing variant JASMONATE ZIM-DOMAIN 9β (JAZ9β) with an intron retention in the Jas motif, which compromises its interaction with CORONATINE INSENSITIVE1 and thus enhances the stability of JAZ9β protein. Moreover, JAZ9β could interact with MYC2 and obstruct its activity, thereby attenuating JA signaling. Correspondingly, overexpression of <i>JAZ9β</i> rescued the early senescence phenotype of the <i>u2b″</i> mutant.</p>\n </li>\n \n \n <li>\n \n <p>Furthermore, JA treatment promoted expression of U2B″ that was found to be a direct target of MYC2. Overexpression of <i>MYC2</i> in the <i>u2b″</i> mutant resulted in a more pronounced premature senescence than that in wild-type plants.</p>\n </li>\n \n \n <li>\n \n <p>Collectively, our findings reveal that the spliceosomal protein U2B″ fine-tunes leaf senescence by enhancing the expression of JAZ9β and thereby attenuating JA signaling.</p>\n </li>\n </ul>\n \n </div>","PeriodicalId":48887,"journal":{"name":"New Phytologist","volume":null,"pages":null},"PeriodicalIF":9.4000,"publicationDate":"2023-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"New Phytologist","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/nph.19198","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Agricultural and Biological Sciences","Score":null,"Total":0}
引用次数: 0

Abstract

  • The regulatory framework of leaf senescence is gradually becoming clearer; however, the fine regulation of this process remains largely unknown.

  • Here, genetic analysis revealed that U2 small nuclear ribonucleoprotein B (U2B″), a component of the spliceosome, is a negative regulator of leaf senescence. Mutation of U2B″ led to precocious leaf senescence, whereas overexpression of U2B″ extended leaf longevity. Transcriptome analysis revealed that the jasmonic acid (JA) signaling pathway was activated in the u2b″ mutant. U2B″ enhances the generation of splicing variant JASMONATE ZIM-DOMAIN 9β (JAZ9β) with an intron retention in the Jas motif, which compromises its interaction with CORONATINE INSENSITIVE1 and thus enhances the stability of JAZ9β protein. Moreover, JAZ9β could interact with MYC2 and obstruct its activity, thereby attenuating JA signaling. Correspondingly, overexpression of JAZ9β rescued the early senescence phenotype of the u2b″ mutant.

  • Furthermore, JA treatment promoted expression of U2B″ that was found to be a direct target of MYC2. Overexpression of MYC2 in the u2b″ mutant resulted in a more pronounced premature senescence than that in wild-type plants.

  • Collectively, our findings reveal that the spliceosomal protein U2B″ fine-tunes leaf senescence by enhancing the expression of JAZ9β and thereby attenuating JA signaling.

剪接体蛋白U2B〃通过增强剪接变异体JAZ9β的表达以减弱拟南芥茉莉酸信号传导来延缓叶片衰老
叶片衰老的调控框架逐渐清晰;然而,这一过程的精细调控在很大程度上仍是未知的。遗传分析表明,剪接体的一个组成部分U2小核核糖核蛋白B(U2B〃)是叶片衰老的负调控因子。U2B〃的突变导致早熟叶片衰老,而U2B〃过表达延长了叶片寿命。转录组分析显示,在u2b〃突变体中茉莉酸(JA)信号通路被激活。U2B〃增强了Jas基序中内含子保留的剪接变体JASMONATE ZIM-DOMAIN 9β(JAZ9β)的产生,这损害了其与CORONATINE INSENSIVE1的相互作用,从而增强了JAZ9?蛋白的稳定性。此外,JAZ9β可以与MYC2相互作用并阻断其活性,从而减弱JA信号传导。相应地,JAZ9β的过表达挽救了u2b〃突变体的早衰表型。此外,JA处理促进U2B〃的表达,U2B〃被发现是MYC2的直接靶点。u2b〃突变体中MYC2的过表达导致比野生型植物更明显的早衰。总之,我们的研究结果表明,剪接体蛋白U2B〃通过增强JAZ9β的表达从而减弱JA信号传导来微调叶片衰老。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
New Phytologist
New Phytologist PLANT SCIENCES-
CiteScore
17.60
自引率
5.30%
发文量
728
审稿时长
1 months
期刊介绍: New Phytologist is a leading publication that showcases exceptional and groundbreaking research in plant science and its practical applications. With a focus on five distinct sections - Physiology & Development, Environment, Interaction, Evolution, and Transformative Plant Biotechnology - the journal covers a wide array of topics ranging from cellular processes to the impact of global environmental changes. We encourage the use of interdisciplinary approaches, and our content is structured to reflect this. Our journal acknowledges the diverse techniques employed in plant science, including molecular and cell biology, functional genomics, modeling, and system-based approaches, across various subfields.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信