AtVQ25 promotes salicylic acid-related leaf senescence by fine-tuning the self-repression of AtWRKY53

IF 9.3 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Qi Tan, Mingming Zhao, Jingwei Gao, Ke Li, Mengwei Zhang, Yunjia Li, Zeting Liu, Yujia Song, Xiaoyue Lu, Zhengge Zhu, Rongcheng Lin, Pengcheng Yin, Chunjiang Zhou, Geng Wang
{"title":"AtVQ25 promotes salicylic acid-related leaf senescence by fine-tuning the self-repression of AtWRKY53","authors":"Qi Tan,&nbsp;Mingming Zhao,&nbsp;Jingwei Gao,&nbsp;Ke Li,&nbsp;Mengwei Zhang,&nbsp;Yunjia Li,&nbsp;Zeting Liu,&nbsp;Yujia Song,&nbsp;Xiaoyue Lu,&nbsp;Zhengge Zhu,&nbsp;Rongcheng Lin,&nbsp;Pengcheng Yin,&nbsp;Chunjiang Zhou,&nbsp;Geng Wang","doi":"10.1111/jipb.13659","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Most mechanistic details of chronologically ordered regulation of leaf senescence are unknown. Regulatory networks centered on AtWRKY53 are crucial for orchestrating and integrating various senescence-related signals. Notably, AtWRKY53 binds to its own promoter and represses transcription of <i>AtWRKY53</i>, but the biological significance and mechanism underlying this self-repression remain unclear. In this study, we identified the VQ motif-containing protein AtVQ25 as a cooperator of AtWRKY53. The expression level of <i>AtVQ25</i> peaked at mature stage and was specifically repressed after the onset of leaf senescence. <i>AtVQ25</i>-overexpressing plants and <i>atvq25</i> mutants displayed precocious and delayed leaf senescence, respectively. Importantly, we identified AtWRKY53 as an interacting partner of AtVQ25. We determined that interaction between AtVQ25 and AtWRKY53 prevented AtWRKY53 from binding to W-box elements on the <i>AtWRKY53</i> promoter and thus counteracted the self-repression of <i>AtWRKY53</i>. In addition, our RNA-sequencing data revealed that the AtVQ25-AtWRKY53 module is related to the salicylic acid (SA) pathway. Precocious leaf senescence and SA-induced leaf senescence in <i>AtVQ25</i>-overexpressing lines were inhibited by an SA pathway mutant, <i>atsid2</i>, and <i>NahG</i> transgenic plants; <i>AtVQ25</i>-overexpressing/<i>atwrky53</i> plants were also insensitive to SA-induced leaf senescence. Collectively, we demonstrated that AtVQ25 directly attenuates the self-repression of <i>AtWRKY53</i> during the onset of leaf senescence, which is substantially helpful for understanding the timing of leaf senescence onset modulated by AtWRKY53.</p></div>","PeriodicalId":195,"journal":{"name":"Journal of Integrative Plant Biology","volume":null,"pages":null},"PeriodicalIF":9.3000,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Integrative Plant Biology","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jipb.13659","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Most mechanistic details of chronologically ordered regulation of leaf senescence are unknown. Regulatory networks centered on AtWRKY53 are crucial for orchestrating and integrating various senescence-related signals. Notably, AtWRKY53 binds to its own promoter and represses transcription of AtWRKY53, but the biological significance and mechanism underlying this self-repression remain unclear. In this study, we identified the VQ motif-containing protein AtVQ25 as a cooperator of AtWRKY53. The expression level of AtVQ25 peaked at mature stage and was specifically repressed after the onset of leaf senescence. AtVQ25-overexpressing plants and atvq25 mutants displayed precocious and delayed leaf senescence, respectively. Importantly, we identified AtWRKY53 as an interacting partner of AtVQ25. We determined that interaction between AtVQ25 and AtWRKY53 prevented AtWRKY53 from binding to W-box elements on the AtWRKY53 promoter and thus counteracted the self-repression of AtWRKY53. In addition, our RNA-sequencing data revealed that the AtVQ25-AtWRKY53 module is related to the salicylic acid (SA) pathway. Precocious leaf senescence and SA-induced leaf senescence in AtVQ25-overexpressing lines were inhibited by an SA pathway mutant, atsid2, and NahG transgenic plants; AtVQ25-overexpressing/atwrky53 plants were also insensitive to SA-induced leaf senescence. Collectively, we demonstrated that AtVQ25 directly attenuates the self-repression of AtWRKY53 during the onset of leaf senescence, which is substantially helpful for understanding the timing of leaf senescence onset modulated by AtWRKY53.

Abstract Image

AtVQ25 通过微调 AtWRKY53 的自我抑制促进与水杨酸相关的叶片衰老
按时间顺序调控叶片衰老的大部分机理细节尚不清楚。以 AtWRKY53 为中心的调控网络对于协调和整合各种衰老相关信号至关重要。值得注意的是,AtWRKY53 与自身启动子结合并抑制 AtWRKY53 的转录,但这种自我抑制的生物学意义和机制仍不清楚。在本研究中,我们发现含 VQ 基序的蛋白 AtVQ25 是 AtWRKY53 的合作者。AtVQ25 的表达水平在成熟期达到峰值,并在叶片开始衰老后受到特异性抑制。AtVQ25过表达植株和atvq25突变体分别表现出叶片提前衰老和延迟衰老。重要的是,我们发现 AtWRKY53 是 AtVQ25 的相互作用伙伴。我们确定 AtVQ25 与 AtWRKY53 之间的相互作用阻止了 AtWRKY53 与 AtWRKY53 启动子上的 W-box 元件结合,从而抵消了 AtWRKY53 的自我抑制作用。此外,我们的 RNA 序列数据显示 AtVQ25-AtWRKY53 模块与水杨酸(SA)途径有关。SA通路突变体atsid2和NahG转基因植株抑制了AtVQ25高表达株系的叶片早衰和SA诱导的叶片衰老;AtVQ25高表达/atwrky53植株对SA诱导的叶片衰老也不敏感。总之,我们证明了在叶片衰老开始时,AtVQ25直接减弱了AtWRKY53的自我抑制,这对理解AtWRKY53调控的叶片衰老开始时间有很大帮助。
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
Journal of Integrative Plant Biology
Journal of Integrative Plant Biology 生物-生化与分子生物学
CiteScore
18.00
自引率
5.30%
发文量
220
审稿时长
3 months
期刊介绍: Journal of Integrative Plant Biology is a leading academic journal reporting on the latest discoveries in plant biology.Enjoy the latest news and developments in the field, understand new and improved methods and research tools, and explore basic biological questions through reproducible experimental design, using genetic, biochemical, cell and molecular biological methods, and statistical analyses.
文献相关原料
公司名称 产品信息 采购帮参考价格
×
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