Zhang Ting, Xu Pengbo, Wang Wenxiu, Wang Sheng, Caruana Julie C, Yang Hong-Quan, Lian Hongli
School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
State Key Laboratory of Genetic Engineering and Collaborative Innovation Center for Genetics and Development, Institute of Plant Biology, School of Life Sciences, Fudan University, Shanghai, China.
Front Plant Sci. 2018 Jan 9;8:2225. doi: 10.3389/fpls.2017.02225. eCollection 2017.
In , brassinosteroids (BR) are major growth-promoting hormones, which integrate with the heterotrimeric guanine nucleotide-binding protein (G-protein) signals and cooperatively modulate cell division and elongation. However, the mechanisms of interaction between BR and G-protein are not well understood. Here, we show that the G-protein β subunit AGB1 directly interacts with the BR transcription factor BES1 and . An AGB1-null mutant, , displays BR hyposensitivity and brassinazole (BRZ, BR biosynthesis inhibitor) hypersensitivity, which suggests that AGB1 positively mediates the BR signaling pathway. Moreover, we demonstrate that AGB1 synergistically regulates expression of BES1 target genes, including the BR biosynthesis genes and and the family genes required for promoting cell elongation. Further, Western blot analysis of BES1 phosphorylation states indicates that the interaction between AGB1 and BES1 alters the phosphorylation status of BES1 and increases the ratio of dephosphorylated to phosphorylated BES1, which leads to accumulation of dephosphorylated BES1 in the nucleus. Finally, AGB1 promotes BES1 binding to BR target genes and stimulates the transcriptional activity of BES1. Taken together, our results demonstrate that AGB1 positively regulates cell elongation by affecting the phosphorylation status and transcriptional activity of BES1.
在植物中，油菜素甾醇（BR）是主要的促进生长激素，它与异源三聚体鸟嘌呤核苷酸结合蛋白（G蛋白）信号整合，并协同调节细胞分裂和伸长。然而，BR与G蛋白之间的相互作用机制尚不清楚。在这里，我们表明G蛋白β亚基AGB1直接与BR转录因子BES1相互作用。一个AGB1缺失突变体表现出对BR的低敏感性和对油菜素唑（BRZ，BR生物合成抑制剂）的高敏感性，这表明AGB1正向介导BR信号通路。此外，我们证明AGB1协同调节BES1靶基因的表达，包括BR生物合成基因以及促进细胞伸长所需的家族基因。进一步的，对BES1磷酸化状态的蛋白质免疫印迹分析表明，AGB1与BES1之间的相互作用改变了BES1的磷酸化状态，并增加了去磷酸化BES1与磷酸化BES1的比例，这导致去磷酸化BES1在细胞核中积累。最后，AGB1促进BES1与BR靶基因的结合，并刺激BES1的转录活性。综上所述，我们的结果表明AGB1通过影响BES1的磷酸化状态和转录活性来正向调节细胞伸长。
