独脚金内酯/MAX2 诱导的油菜素甾醇转录效应物 BES1 的降解调节分枝。
Strigolactone/MAX2-induced degradation of brassinosteroid transcriptional effector BES1 regulates shoot branching.
机构信息
State Key Laboratory of Genetic Engineering and Institute of Plant Biology, School of Life Sciences, Fudan University, 200433 Shanghai, PRC.
School of Agriculture and Biology, Shanghai Jiao Tong University, 200240 Shanghai, PRC.
出版信息
Dev Cell. 2013 Dec 23;27(6):681-8. doi: 10.1016/j.devcel.2013.11.010.
Strigolactones (SLs), a class of the most recently identified terpenoid phytohormones, play essential roles in plant development, specifically in suppressing shoot branching. MAX2, a subunit of an SCF E3 ligase and a positive regulator that inhibits shoot branching, is likely a key SL signaling component. Here, we provide genetic and biochemical evidence to demonstrate that BES1 interacts with MAX2 and acts as its substrate to regulate SL-responsive gene expression. Additional AtD14, a putative receptor of SLs, can promote BES1 degradation. Knockdown of BES1 and its homologs dramatically suppressed the branching phenotype of max2-1 mutant. These results portray an SL signaling cascade from the putative receptor to downstream transcription factors. In addition, we demonstrate that the SL and brassinosteroid (BR) signaling pathways distinctly regulate the same transcription factor, BES1, to control specific developmental processes.
独脚金内酯（SLs）是最近发现的萜类植物激素中的一类，在植物发育中起着至关重要的作用，特别是在抑制侧芽分枝方面。MAX2 是 SCF E3 连接酶的一个亚基，是一种正向调控因子，可抑制侧芽分枝，很可能是 SL 信号传导的关键成分。在这里，我们提供遗传和生化证据表明 BES1 与 MAX2 相互作用，并作为其底物来调节 SL 响应基因的表达。另外，AtD14，一种可能的 SL 受体，能够促进 BES1 的降解。BES1 和其同源物的敲低显著抑制了 max2-1 突变体的分枝表型。这些结果描绘了一个从假定受体到下游转录因子的 SL 信号级联。此外，我们证明 SL 和油菜素内酯（BR）信号通路分别调节相同的转录因子 BES1，以控制特定的发育过程。
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