Strigolactone/MAX2-Induced Degradation of Brassinosteroid Transcriptional Effector BES1 Regulates Shoot Branching
Strigolactone/MAX2-Induced Degradation of Brassinosteroid Transcriptional Effector BES1 Regulates Shoot Branching
复制标题
独脚金内酯/MAX2 诱导的油菜素类固醇转录效应子 BES1 降解调节芽分枝
DOI：
10.1016/j.devcel.2013.11.010
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发表时间：
2013-12-23
影响因子：
11.8
通讯作者：
Wang, Xuelu
中科院分区：
文献类型：
--
作者：
Wang, Yuan;Sun, Shiyong;Wang, Xuelu
独脚金内酯（SL）是一类新近发现的萜类植物激素，在植物生长发育中起着重要作用，特别是抑制枝条分枝。MAX2是SCF E3连接酶的一个亚基，也是一个抑制芽分枝的正调控因子，可能是SL信号传导的关键成分。在这里，我们提供的遗传和生化证据表明，BES 1与MAX 2相互作用，并作为其基板，以调节SL响应基因的表达。另外的AtD 14，SL的假定受体，可以促进BES 1降解。敲除BES 1及其同源物显著抑制了max 2 -1突变体的分支表型。这些结果描绘了从推定的受体到下游转录因子的SL信号级联。此外，我们表明，SL和油菜素类固醇（BR）信号通路明显调节相同的转录因子，BES 1，控制特定的发育过程。
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.