Wang Lijun, Cheng Hua, Wang Qi, Si Chaona, Yang Yiman, Yu Yao, Zhou Lijie, Ding Lian, Song Aiping, Xu Dongqing, Chen Sumei, Fang Weimin, Chen Fadi, Jiang Jiafu
State Key Laboratory of Crop Genetics and Germplasm Enhancement, Key Laboratory of Landscaping, Ministry of Agriculture and Rural Affairs, Key Laboratory of Biology of Ornamental Plants in East China, National Forestry and Grassland Administration, College of Horticulture, Nanjing Agricultural University, Nanjing, 210095, China.
College of Landscape and Ecological Engineering, Hebei University of Engineering, Handan, 056038, China.
Hortic Res. 2021 Apr 1;8(1):79. doi: 10.1038/s41438-021-00516-z.
The CmBBX8-CmFTL1 regulatory module is a key determinant in the transition from vegetative growth to reproductive development in summer-flowering chrysanthemum. However, the detailed regulatory mechanism of CmBBX8-mediated flowering remains elusive. In this study, we revealed that RADICAL-INDUCED CELL DEATH 1 (CmRCD1) physically associated with CmBBX8 through bimolecular fluorescence complementation (BiFC), pulldown and Coimmunoprecipitation (CoIP) assays. Furthermore, the RCD1-SRO1-TAF4 (RST) domain of CmRCD1 and the B-box of CmBBX8 mediated their interaction. In addition, Luciferase (LUC) assays and electrophoretic mobility shift assay (EMSAs) showed that CmRCD1 repressed the transcriptional activity of CmBBX8 and interfered with its binding to the CmFTL1 promoter, thereby leading to delayed flowering in the summer chrysanthemum 'Yuuka'. These results provide insight into the molecular framework of CmRCD1-CmBBX8-mediated flowering in chrysanthemum.
CmBBX8-CmFTL1调控模块是夏菊从营养生长向生殖发育转变的关键决定因素。然而，CmBBX8介导开花的详细调控机制仍不清楚。在本研究中，我们通过双分子荧光互补（BiFC）、下拉和免疫共沉淀（CoIP）实验揭示了自由基诱导细胞死亡1（CmRCD1）与CmBBX8存在物理相互作用。此外，CmRCD1的RCD1-SRO1-TAF4（RST）结构域和CmBBX8的B-盒介导了它们之间的相互作用。另外，荧光素酶（LUC）实验和电泳迁移率变动分析（EMSA）表明，CmRCD1抑制了CmBBX8的转录活性，并干扰其与CmFTL1启动子的结合，从而导致夏菊‘优香’开花延迟。这些结果为菊花中CmRCD1-CmBBX8介导开花的分子框架提供了见解。
