水稻特异性miR1850.1靶向NPR3调控冷胁迫反应。

IF 9.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yang Shen, Xiaoxi Cai, Wanhong Li, Hao Wu, Bowei Jia, Mingzhe Sun, Xiaoli Sun
{"title":"水稻特异性miR1850.1靶向NPR3调控冷胁迫反应。","authors":"Yang Shen, Xiaoxi Cai, Wanhong Li, Hao Wu, Bowei Jia, Mingzhe Sun, Xiaoli Sun","doi":"10.1016/j.xplc.2025.101324","DOIUrl":null,"url":null,"abstract":"<p><p>Cold stress in temperate rice production regions is responsible for yield losses of up to 30-40%, and improving cold tolerance is a practical strategy to safeguard rice production. Numerous genes and signaling networks for cold stress have been identified in rice. However, little is known about the roles of microRNAs in the cold stress response. Here, we find that a rice-specific pri-miR1850 and its two mature products, miR1850.1 and miR1850.2, are down-regulated by cold stress. Using gain- and loss-of-function genetic approaches in elite japonica cultivars, we show that pri-miR1850 and miR1850.1 negatively regulate cold tolerance at both the young-seedling and booting stages. miR1850.1 targets and suppresses the immune gene NPR3 by mediating transcript cleavage and transitional repression. Upon cold treatment, NPR3 transcripts and proteins are up-regulated due to the alleviation of miR1850.1-mediated repression and the activation of NPR3 transcription. miR1850.1 functions genetically through NPR3 in the cold-stress response. The miR1850.1-NPR3 module also controls rice disease resistance and grain yields. Our findings reveal a cold-signaling network and provide targets for engineering cold-tolerant japonica varieties to endure fluctuating future climates.</p>","PeriodicalId":52373,"journal":{"name":"Plant Communications","volume":" ","pages":"101324"},"PeriodicalIF":9.4000,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Rice-specific miR1850.1 targets NPR3 to regulate cold stress response.\",\"authors\":\"Yang Shen, Xiaoxi Cai, Wanhong Li, Hao Wu, Bowei Jia, Mingzhe Sun, Xiaoli Sun\",\"doi\":\"10.1016/j.xplc.2025.101324\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Cold stress in temperate rice production regions is responsible for yield losses of up to 30-40%, and improving cold tolerance is a practical strategy to safeguard rice production. Numerous genes and signaling networks for cold stress have been identified in rice. However, little is known about the roles of microRNAs in the cold stress response. Here, we find that a rice-specific pri-miR1850 and its two mature products, miR1850.1 and miR1850.2, are down-regulated by cold stress. Using gain- and loss-of-function genetic approaches in elite japonica cultivars, we show that pri-miR1850 and miR1850.1 negatively regulate cold tolerance at both the young-seedling and booting stages. miR1850.1 targets and suppresses the immune gene NPR3 by mediating transcript cleavage and transitional repression. Upon cold treatment, NPR3 transcripts and proteins are up-regulated due to the alleviation of miR1850.1-mediated repression and the activation of NPR3 transcription. miR1850.1 functions genetically through NPR3 in the cold-stress response. The miR1850.1-NPR3 module also controls rice disease resistance and grain yields. Our findings reveal a cold-signaling network and provide targets for engineering cold-tolerant japonica varieties to endure fluctuating future climates.</p>\",\"PeriodicalId\":52373,\"journal\":{\"name\":\"Plant Communications\",\"volume\":\" \",\"pages\":\"101324\"},\"PeriodicalIF\":9.4000,\"publicationDate\":\"2025-03-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Plant Communications\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/j.xplc.2025.101324\",\"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}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Plant Communications","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.xplc.2025.101324","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

摘要

在温带水稻产区,冷胁迫造成的产量损失高达 30-40%,因此提高耐寒性是保障水稻产量的一项切实可行的策略。在水稻中已经发现了许多抗寒基因和信号网络。然而,人们对 microRNA 在冷胁迫响应中的作用知之甚少。在这里,我们发现水稻特有的 pri-miR1850 及其两个成熟产物 miR1850.1 和 miR1850.2 在冷胁迫下会下调。我们在粳稻精英栽培品种中采用功能增益和功能缺失的遗传方法,结果表明 pri-miR1850 和 miR1850.1 对幼苗和出苗阶段的耐寒性有负面调节作用。miR1850.1 通过介导转录本裂解和过渡抑制,靶向并抑制免疫基因 NPR3。冷处理后,由于 miR1850.1 介导的抑制作用减弱和 NPR3 转录激活,NPR3 转录本和蛋白质上调。miR1850.1 通过 NPR3 在冷应激反应中发挥遗传功能。miR1850.1-NPR3 模块还控制着水稻的抗病性和谷物产量。我们的研究结果揭示了一个冷信号网络,并为培育耐寒粳稻品种提供了目标,以适应未来多变的气候。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Rice-specific miR1850.1 targets NPR3 to regulate cold stress response.

Cold stress in temperate rice production regions is responsible for yield losses of up to 30-40%, and improving cold tolerance is a practical strategy to safeguard rice production. Numerous genes and signaling networks for cold stress have been identified in rice. However, little is known about the roles of microRNAs in the cold stress response. Here, we find that a rice-specific pri-miR1850 and its two mature products, miR1850.1 and miR1850.2, are down-regulated by cold stress. Using gain- and loss-of-function genetic approaches in elite japonica cultivars, we show that pri-miR1850 and miR1850.1 negatively regulate cold tolerance at both the young-seedling and booting stages. miR1850.1 targets and suppresses the immune gene NPR3 by mediating transcript cleavage and transitional repression. Upon cold treatment, NPR3 transcripts and proteins are up-regulated due to the alleviation of miR1850.1-mediated repression and the activation of NPR3 transcription. miR1850.1 functions genetically through NPR3 in the cold-stress response. The miR1850.1-NPR3 module also controls rice disease resistance and grain yields. Our findings reveal a cold-signaling network and provide targets for engineering cold-tolerant japonica varieties to endure fluctuating future climates.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Plant Communications
Plant Communications Agricultural and Biological Sciences-Plant Science
CiteScore
15.70
自引率
5.70%
发文量
105
审稿时长
6 weeks
期刊介绍: Plant Communications is an open access publishing platform that supports the global plant science community. It publishes original research, review articles, technical advances, and research resources in various areas of plant sciences. The scope of topics includes evolution, ecology, physiology, biochemistry, development, reproduction, metabolism, molecular and cellular biology, genetics, genomics, environmental interactions, biotechnology, breeding of higher and lower plants, and their interactions with other organisms. The goal of Plant Communications is to provide a high-quality platform for the dissemination of plant science research.
×
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