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作 者: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
机构地区:[1]Key Laboratory of Tobacco Gene Resources,Tobacco Research Institute,Chinese Academy of Agricultural Sciences(CAAS),Qingdao,266101 China [2]College of Plant Protection,Shenyang Agricultural University,Shenyang,110866 China [3]Luzhou Tobacco Company of Sichuan Province,Luzhou,646000 China
出 处:《Journal of Integrative Plant Biology》2022年第9期1673-1689,共17页植物学报(英文版)
基 金:supported by the National Natural Science Foundation of China(31600237);the Agricultural Science and Technology Innovation Program(ASTIP-TRIC02);the Key Science and Technology Projects of Sichuan Tobacco Institute(SCYC202002);the Central Public-Interest Scientific Institution Basal Research Fund(16102320200002)。
摘 要: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-RESPONSIVEELEMENTBINDING 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 ERF4promotes 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.
关 键 词:ARABIDOPSIS cell growth CYCA2 3 ENDOREDUPLICATION ERF4 TCP15
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