The AGAMOUS-LIKE 16–GENERAL REGULATORY FACTOR 1 module regulates axillary bud outgrowth via catabolism of abscisic acid in cucumber

Jiacai Chen, Liu Liu, Guanghui Wang, Guangxin Chen, Xiaofeng Liu, Min Li, Lijie Han, Weiyuan Song, Shaoyun Wang, Chuang Li, Zhongyi Wang, Yuxiang Huang, Chaoheng Gu, Zhengan Yang, Zhaoyang Zhou, Jianyu Zhao, Xiaolan Zhang
{"title":"The AGAMOUS-LIKE 16–GENERAL REGULATORY FACTOR 1 module regulates axillary bud outgrowth via catabolism of abscisic acid in cucumber","authors":"Jiacai Chen, Liu Liu, Guanghui Wang, Guangxin Chen, Xiaofeng Liu, Min Li, Lijie Han, Weiyuan Song, Shaoyun Wang, Chuang Li, Zhongyi Wang, Yuxiang Huang, Chaoheng Gu, Zhengan Yang, Zhaoyang Zhou, Jianyu Zhao, Xiaolan Zhang","doi":"10.1093/plcell/koae108","DOIUrl":null,"url":null,"abstract":"Lateral branches are important components of shoot architecture and directly affect crop yield and production cost. Although sporadic studies have implicated abscisic acid (ABA) biosynthesis in axillary bud outgrowth, the function of ABA catabolism and its upstream regulators in shoot branching remain elusive. Here, we showed that the MADS-box transcription factor AGAMOUS-LIKE 16 (CsAGL16) is a positive regulator of axillary bud outgrowth in cucumber (Cucumis sativus). Functional disruption of CsAGL16 led to reduced bud outgrowth, whereas overexpression of CsAGL16 resulted in enhanced branching. CsAGL16 directly binds to the promoter of the ABA 8'-hydroxylase gene CsCYP707A4 and promotes its expression. Loss of CsCYP707A4 function inhibited axillary bud outgrowth and increased ABA levels. Elevated expression of CsCYP707A4 or treatment with an ABA biosynthesis inhibitor largely rescued the Csagl16 mutant phenotype. Moreover, cucumber General Regulatory Factor 1 (CsGRF1) interacts with CsAGL16 and antagonizes CsAGL16-mediated CsCYP707A4 activation. Disruption of CsGRF1 resulted in elongated branches and decreased ABA levels in the axillary buds. The Csagl16 Csgrf1 double mutant exhibited a branching phenotype resembling that of the Csagl16 single mutant. Therefore, our data suggest that the CsAGL16–CsGRF1 module regulates axillary bud outgrowth via CsCYP707A4-mediated ABA catabolism in cucumber. Our findings provide a strategy to manipulate ABA levels in axillary buds during crop breeding to produce desirable branching phenotypes.","PeriodicalId":501012,"journal":{"name":"The Plant Cell","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Plant Cell","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/plcell/koae108","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Lateral branches are important components of shoot architecture and directly affect crop yield and production cost. Although sporadic studies have implicated abscisic acid (ABA) biosynthesis in axillary bud outgrowth, the function of ABA catabolism and its upstream regulators in shoot branching remain elusive. Here, we showed that the MADS-box transcription factor AGAMOUS-LIKE 16 (CsAGL16) is a positive regulator of axillary bud outgrowth in cucumber (Cucumis sativus). Functional disruption of CsAGL16 led to reduced bud outgrowth, whereas overexpression of CsAGL16 resulted in enhanced branching. CsAGL16 directly binds to the promoter of the ABA 8'-hydroxylase gene CsCYP707A4 and promotes its expression. Loss of CsCYP707A4 function inhibited axillary bud outgrowth and increased ABA levels. Elevated expression of CsCYP707A4 or treatment with an ABA biosynthesis inhibitor largely rescued the Csagl16 mutant phenotype. Moreover, cucumber General Regulatory Factor 1 (CsGRF1) interacts with CsAGL16 and antagonizes CsAGL16-mediated CsCYP707A4 activation. Disruption of CsGRF1 resulted in elongated branches and decreased ABA levels in the axillary buds. The Csagl16 Csgrf1 double mutant exhibited a branching phenotype resembling that of the Csagl16 single mutant. Therefore, our data suggest that the CsAGL16–CsGRF1 module regulates axillary bud outgrowth via CsCYP707A4-mediated ABA catabolism in cucumber. Our findings provide a strategy to manipulate ABA levels in axillary buds during crop breeding to produce desirable branching phenotypes.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
类似 AGAMOUS 的 16 种元素调控因子 1 模块通过脱落酸的分解来调控黄瓜腋芽的生长
侧枝是芽结构的重要组成部分,直接影响作物产量和生产成本。尽管零星的研究表明脱落酸(ABA)的生物合成与腋芽的生长有关,但 ABA 分解及其上游调控因子在芽分枝中的功能仍然难以确定。在这里,我们发现 MADS-box 转录因子 AGAMOUS-LIKE 16(CsAGL16)是黄瓜(Cucumis sativus)腋芽生长的正调控因子。CsAGL16 的功能性破坏会导致芽的生长减弱,而过表达 CsAGL16 则会导致分枝增强。CsAGL16 直接与 ABA 8'-hydroxylase 基因 CsCYP707A4 的启动子结合并促进其表达。CsCYP707A4 功能的缺失会抑制腋芽的生长并增加 ABA 水平。提高 CsCYP707A4 的表达或用 ABA 生物合成抑制剂处理在很大程度上能挽救 Csagl16 突变体的表型。此外,黄瓜综合调节因子 1(CsGRF1)与 CsAGL16 相互作用,并拮抗 CsAGL16 介导的 CsCYP707A4 激活。干扰 CsGRF1 会导致枝条伸长,腋芽中的 ABA 水平降低。Csagl16 Csgrf1 双突变体的分枝表型与 Csagl16 单突变体相似。因此,我们的数据表明,CsAGL16-CsGRF1 模块通过 CsCYP707A4 介导的 ABA 分解作用调节黄瓜腋芽的生长。我们的发现为在作物育种过程中操纵腋芽中的 ABA 水平以产生理想的分枝表型提供了一种策略。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
The FERONIA–RESPONSIVE TO DESSICATION 26 module regulates vascular immunity to Ralstonia solanacearum Phosphoketolase and KDPG aldolase metabolisms modulate photosynthetic carbon yield in cyanobacteria The kinase ATR controls meiotic crossover distribution at the genome scale in Arabidopsis Ribosome binding of phasiRNA precursors accelerates the 24-nt phasiRNA burst in meiotic maize anthers EMBRYONIC FLOWER 1 regulates male reproduction by repressing the jasmonate pathway downstream transcription factor MYB26
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1