ERF4 interacts with and antagonizes TCP15 in regulating endoreduplication and cell growth in Arabidopsis

内复制 生物 细胞生物学 有丝分裂 拟南芥 细胞周期 转录因子 调节器 抑制因子 细胞分裂 E2F型 转录调控 细胞生长 遗传学 细胞 基因 突变体
作者
Anming Ding,Chuantao Xu,Qiang Xie,M. Zhang,Yan Ning,Changbo Dai,Jing Lv,Mengmeng Cui,Wei‐Feng Wang,Yanfa Sun
出处
期刊:Journal of Integrative Plant Biology [Wiley]
卷期号:64 (9): 1673-1689 被引量:12
标识
DOI:10.1111/jipb.13323
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-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.
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