Li Yuting, Xiong Hongchun, Guo Huijun, Xie Yongdun, Zhao Linshu, Gu Jiayu, Li Huiyuan, Zhao Shirong, Ding Yuping, Zhou Chunyun, Fang Zhengwu, Liu Luxiang
State Key Laboratory of Crop Gene Resources and Breeding/National Engineering Laboratory of Crop Molecular Breeding/CAEA Research and Development Centre on Nuclear Technology Applications for Irradiation Mutation Breeding, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing, 100081, China.
MARA Key Laboratory of Sustainable Crop Production in the Middle Reaches of the Yangtze River (co-construction by Ministry and Province), College of Agriculture, Yangtze University, Jingzhou, 434025, China.
Plant Biotechnol J. 2025 Jan;23(1):20-35. doi: 10.1111/pbi.14474. Epub 2024 Sep 14.
Vernalization and photoperiod pathways converging at FT1 control the transition to flowering in wheat. Here, we identified a gain-of-function mutation in FT-D1 that results in earlier heading date (HD), and shorter plant height and spike length in the gamma ray-induced eh1 wheat mutant. Knockout of the wild-type and overexpression of the mutated FT-D1 indicate that both alleles are functional to affect HD and plant height. Protein interaction assays demonstrated that the frameshift mutation in FT-D1 exon 3 led to gain-of-function interactions with 14-3-3A and FDL6, thereby enabling the formation of florigen activation complex (FAC) and consequently activating a flowering-related transcriptomic programme. This mutation did not affect FT-D1 interactions with TaNaKR5 or TaFTIP7, both of which could modulate HD, potentially via mediating FT-D1 translocation to the shoot apical meristem. Furthermore, the 'Segment B' external loop is essential for FT-D1 interaction with FDL6, while residue Y85 is required for interactions with TaNaKR5 and TaFTIP7. Finally, the flowering regulatory hub gene, ELF5, was identified as the FT-D1 regulatory target. This study illustrates FT-D1 function in determining wheat HD with a suite of interaction partners and provides genetic resources for tuning HD in elite wheat lines.
春化途径和光周期途径在FT1处汇聚,控制着小麦向开花的转变。在此,我们在FT-D1中鉴定出一个功能获得性突变,该突变导致γ射线诱导的eh1小麦突变体抽穗期提前、株高和穗长缩短。野生型基因敲除和突变型FT-D1过表达表明,这两个等位基因均对抽穗期和株高有影响。蛋白质相互作用分析表明,FT-D1第3外显子的移码突变导致其与14-3-3A和FDL6发生功能获得性相互作用,从而形成成花素激活复合体(FAC),进而激活与开花相关的转录组程序。该突变不影响FT-D1与TaNaKR5或TaFTIP7的相互作用,这两者可能通过介导FT-D1向茎尖分生组织的转运来调节抽穗期。此外,“B段”外环对于FT-D1与FDL6的相互作用至关重要,而残基Y85是与TaNaKR5和TaFTIP7相互作用所必需的。最后,开花调控枢纽基因ELF5被鉴定为FT-D1的调控靶点。本研究阐明了FT-D1与一系列相互作用伙伴在决定小麦抽穗期方面的功能,并为优化优良小麦品系的抽穗期提供了遗传资源。