J Integr Plant Biol. ›› 2022, Vol. 64 ›› Issue (9): 1673-1689.DOI: 10.1111/jipb.13323

• Cell and Developmental Biology • Previous Articles     Next Articles

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

An‐Ming Ding1*, Chuan‐Tao Xu2,3, Qiang Xie3, Ming‐Jin Zhang3, Ning Yan1*, Chang‐Bo Dai1, Jing Lv1, Meng‐Meng Cui1, Wei‐Feng Wang1 and Yu‐He Sun1   

  1. 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

    Correspondences: An‐Ming Ding (dinganming@caas.cn, Dr. Ding is fully responsible for the distributions of the materials associated with this article); Ning Yan (yanning@caas.cn)
  • Received:2022-04-20 Accepted:2022-06-29 Online:2022-07-29 Published:2022-09-01


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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