An-Ming Ding, Chuan-Tao Xu, Qiang Xie, Ming-Jin Zhang, Ning Yan, Chang-Bo Dai, Jing Lv, Meng-Meng Cui, Wei-Feng Wang, Yu-He Sun
{"title":"ERF4与TCP15相互作用并拮抗TCP15调控拟南芥内复制和细胞生长","authors":"An-Ming Ding, Chuan-Tao Xu, Qiang Xie, Ming-Jin Zhang, Ning Yan, Chang-Bo Dai, Jing Lv, Meng-Meng Cui, Wei-Feng Wang, Yu-He Sun","doi":"10.1111/jipb.13323","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Endoreduplication is prevalent during plant growth and development, and is often correlated with large cell and organ size. Despite its prevalence, the transcriptional regulatory mechanisms underlying the transition from mitotic cell division to endoreduplication remain elusive. Here, we characterize ETHYLENE-RESPONSIVE ELEMENT BINDING FACTOR 4 (ERF4) as a positive regulator of endoreduplication through its function as a transcriptional repressor. <i>ERF4</i> was specifically expressed in mature tissues in which the cells were undergoing expansion, but was rarely expressed in young organs. Plants overexpressing <i>ERF4</i> exhibited much larger cells and organs, while plants that lacked functional <i>ERF4</i> displayed smaller organs than the wild-type. <i>ERF4</i> was further shown to regulate cell size by controlling the endopolyploidy level in the nuclei. Moreover, ERF4 physically associates with the class I TEOSINTE BRANCHED 1/CYCLOIDEA/PCF (TCP) protein TCP15, a transcription factor that inhibits endoreduplication by activating the expression of a key cell-cycle gene, <i>CYCLIN A2;3</i> (<i>CYCA2;3</i>). A molecular and genetic analysis revealed that ERF4 promotes endoreduplication by directly suppressing the expression of <i>CYCA2;3</i>. Together, this study demonstrates that ERF4 and TCP15 function as a module to antagonistically regulate each other's activity in regulating downstream genes, thereby controlling the switch from the mitotic cell cycle to endoreduplication during leaf development. These findings expand our understanding of how the control of the cell cycle is fine-tuned by an ERF4–TCP15 transcriptional complex.</p></div>","PeriodicalId":195,"journal":{"name":"Journal of Integrative Plant Biology","volume":null,"pages":null},"PeriodicalIF":9.3000,"publicationDate":"2022-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"6","resultStr":"{\"title\":\"ERF4 interacts with and antagonizes TCP15 in regulating endoreduplication and cell growth in Arabidopsis\",\"authors\":\"An-Ming Ding, Chuan-Tao Xu, Qiang Xie, Ming-Jin Zhang, Ning Yan, Chang-Bo Dai, Jing Lv, Meng-Meng Cui, Wei-Feng Wang, Yu-He Sun\",\"doi\":\"10.1111/jipb.13323\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>Endoreduplication is prevalent during plant growth and development, and is often correlated with large cell and organ size. Despite its prevalence, the transcriptional regulatory mechanisms underlying the transition from mitotic cell division to endoreduplication remain elusive. Here, we characterize ETHYLENE-RESPONSIVE ELEMENT BINDING FACTOR 4 (ERF4) as a positive regulator of endoreduplication through its function as a transcriptional repressor. <i>ERF4</i> was specifically expressed in mature tissues in which the cells were undergoing expansion, but was rarely expressed in young organs. Plants overexpressing <i>ERF4</i> exhibited much larger cells and organs, while plants that lacked functional <i>ERF4</i> displayed smaller organs than the wild-type. <i>ERF4</i> was further shown to regulate cell size by controlling the endopolyploidy level in the nuclei. Moreover, ERF4 physically associates with the class I TEOSINTE BRANCHED 1/CYCLOIDEA/PCF (TCP) protein TCP15, a transcription factor that inhibits endoreduplication by activating the expression of a key cell-cycle gene, <i>CYCLIN A2;3</i> (<i>CYCA2;3</i>). A molecular and genetic analysis revealed that ERF4 promotes endoreduplication by directly suppressing the expression of <i>CYCA2;3</i>. Together, this study demonstrates that ERF4 and TCP15 function as a module to antagonistically regulate each other's activity in regulating downstream genes, thereby controlling the switch from the mitotic cell cycle to endoreduplication during leaf development. These findings expand our understanding of how the control of the cell cycle is fine-tuned by an ERF4–TCP15 transcriptional complex.</p></div>\",\"PeriodicalId\":195,\"journal\":{\"name\":\"Journal of Integrative Plant Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":9.3000,\"publicationDate\":\"2022-06-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Integrative Plant Biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/jipb.13323\",\"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":"Journal of Integrative Plant Biology","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jipb.13323","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}
ERF4 interacts with and antagonizes TCP15 in regulating endoreduplication and cell growth in Arabidopsis
Endoreduplication is prevalent during plant growth and development, and is often correlated with large cell and organ size. Despite its prevalence, the transcriptional regulatory mechanisms underlying the transition from mitotic cell division to endoreduplication remain elusive. Here, we characterize ETHYLENE-RESPONSIVE ELEMENT BINDING FACTOR 4 (ERF4) as a positive regulator of endoreduplication through its function as a transcriptional repressor. ERF4 was specifically expressed in mature tissues in which the cells were undergoing expansion, but was rarely expressed in young organs. Plants overexpressing ERF4 exhibited much larger cells and organs, while plants that lacked functional ERF4 displayed smaller organs than the wild-type. ERF4 was further shown to regulate cell size by controlling the endopolyploidy level in the nuclei. Moreover, ERF4 physically associates with the class I TEOSINTE BRANCHED 1/CYCLOIDEA/PCF (TCP) protein TCP15, a transcription factor that inhibits endoreduplication by activating the expression of a key cell-cycle gene, CYCLIN A2;3 (CYCA2;3). A molecular and genetic analysis revealed that ERF4 promotes endoreduplication by directly suppressing the expression of CYCA2;3. Together, this study demonstrates that ERF4 and TCP15 function as a module to antagonistically regulate each other's activity in regulating downstream genes, thereby controlling the switch from the mitotic cell cycle to endoreduplication during leaf development. These findings expand our understanding of how the control of the cell cycle is fine-tuned by an ERF4–TCP15 transcriptional complex.
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.