Multiple Ways of BES1/BZR1 Degradation to Decode Distinct Developmental and Environmental Cues in Plants.
Multiple Ways of BES1/BZR1 Degradation to Decode Distinct Developmental and Environmental Cues in Plants.
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BES1/BZR1 降解的多种方式可解码植物中独特的发育和环境线索。
DOI：
10.1016/j.molp.2017.06.005
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发表时间：
2017-07
期刊：
影响因子：
27.5
通讯作者：
Xuelu Wang
中科院分区：
文献类型：
--
作者：
Mengran Yang;Xuelu Wang
植物必须不断整合各种环境刺激和多种内源激素以优化其生长发育。BRI 1-EMS-SUPPOR 1（BES 1）和BRASSINAZOLE RESISTANT 1（BZR 1）不仅作为油菜素类固醇（BR）信号传导途径中的关键转录因子，而且作为整合多种信号以调节植物发育和环境适应性的枢纽（Wang et al.，2014年）。BES 1和BZR 1都是通过组成型激活BR信号的突变体的正向遗传筛选鉴定的。功能获得性bes 1-D和bzr 1-D突变体表现出组成型BR应答，并且bes 1-D和bzr 1-D蛋白分别与野生型BES 1和BZR 1相比显示出显著增加的稳定性（He et al.，2002; Yin等人，2002），表明BES 1/BZR 1的稳定性对其功能至关重要。然而，在发现BES 1/BZR 1十多年后，只有有限的信息可以解释BES 1/BZR 1稳定性是如何调节的。已知BES 1/BZR 1的磷酸化状态响应于BR而快速变化，其已被广泛用于确定BR信号传导输出。油菜甾醇不敏感2（BIN 2）激酶磷酸化并抑制BES 1/BZR 1的活性（He等人，2002; Yin等人，2002），而蛋白磷酸酶2A（PP 2A）去磷酸化并激活BES 1/BZR 1（Tang et al.，2011年）。长期以来一直认为BES 1/BZR 1的降解主要依赖于它们的磷酸化并通过26 S蛋白酶体（He et al.，2002; Yin等人，2013年，Wang等报道了一种直接的BES 1降解机制，其中BES 1作为MORE AXILLARY GROWTH LOCUS 2（MAX 2）的底物，MAX 2是一种对独脚金内酯（SL）信号传导至关重要的F盒蛋白，调节拟南芥中的芽分枝（图1，左）。发现bes 1-D突变体具有增加的分支数目并且对SL不敏感。BES 1及其同源物直接与MAX2相互作用，并被MAX2泛素化和降解，MAX2是Skp-CULLIN-F-box（SCF）E3泛素连接酶复合物的亚基。同时，MAX 2介导的BES 1降解被SL处理促进（Wang等人，2013年）。此外，遗传数据显示，敲低BES 1及其同源物抑制了max 2 -1的分支表型，表明BES 1对于MAX 2下游的SL控制的分支是必需的（Wang et al.，2013年）。有趣的是，磷酸化和去磷酸化的BES 1都可以与MAX2相互作用并被MAX2降解。因此，MAX 2介导的BES 1的组织特异性（木质部薄壁细胞）降解控制了一个独特的发育过程，即枝条分枝，
Plants must constantly integrate various environment stimuli and many endogenous hormones to optimize their growth and development. BRI1-EMS-SUPPRESSOR 1 (BES1) and BRASSINAZOLE RESISTANT 1 (BZR1) act not only as key transcription factors in the brassinosteroid (BR) signaling pathway, but also as a hub that integrates diverse signals to regulate plant development and environment adaptability (Wang et al., 2014). Both BES1 and BZR1 were identified through forward genetic screens of mutants with constitutively activated BR signaling. The gain-of-function bes1-D and bzr1-D mutants exhibit constitutive BR responses, and the bes1-D and bzr1-D proteins show significantly increased stability compared with the wild-type BES1 and BZR1, respectively (He et al., 2002; Yin et al., 2002), indicating that the stability of BES1/BZR1 is critical for their function. However, more than a decade after the identification of BES1/BZR1, only limited information is available to explain how BES1/BZR1 stability is regulated. It is known that the phosphorylation status of BES1/BZR1 changes rapidly in response to BRs, which has been widely used to determine BR signaling outputs. The BRASSINOSTEROID INSENSITIVE 2 (BIN2) kinase phosphorylates and inhibits the activity of BES1/BZR1 (He et al., 2002; Yin et al., 2002), whereas the protein phosphatase 2A (PP2A) dephosphorylates and activates BES1/BZR1 (Tang et al., 2011). It has long been assumed that the degradation of BES1/BZR1 is mainly dependent on their phosphorylation and through the 26S proteasome (He et al., 2002; Yin et al., 2002), but several recent studies demonstrated that the regulation of BES1/BZR1 stability is more diverse and far more complicated than what we previously thought.In 2013, Wang et al. reported a direct BES1-degradation mechanism, whereby BES1 serves as the substrate of MORE AXILLARY GROWTH LOCUS 2 (MAX2), an F-box protein critical for strigolactone (SL) signaling, to regulate shoot branching in Arabidopsis (Figure 1, left). It was found that the bes1-D mutant has increased branch number and is insensitive to SLs. BES1 and its homologs directly interact with MAX2 and are ubiquitinated and degraded by MAX2, a subunit of the Skp-CULLIN-F-box (SCF) E3 ubiquitin ligase complex. Meanwhile, the MAX2-mediated BES1 degradation is promoted by SL treatment (Wang et al., 2013). Furthermore, genetic data showed that knockdown of BES1 and its homologs suppressed the branching phenotype of max2-1, suggesting that BES1 is essential for SL-controlled branching in the downstream of MAX2 (Wang et al., 2013). Interestingly, both phosphorylated and dephosphorylated BES1 can interact with and be degraded by MAX2. Thus, the MAX2-mediated tissuespecific (xylem parenchyma cells) degradation of BES1 controls a distinct developmental process, shoot branching, from
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影响因子：
2.4
作者：
Bennett T;Liang Y;Seale M;Ward S;Müller D;Leyser O
通讯作者：
Leyser O
影响因子：
9.2
作者：
Zhang, Zhenzhen;Zhu, Jia-Ying;Roh, Jeehee;Marchive, Chloe;Kim, Seong-Ki;Meyer, Christian;Sun, Yu;Wang, Wenfei;Wang, Zhi-Yong
通讯作者：
Wang, Zhi-Yong
SINAT E3 连接控制拟南芥中油菜素类固醇激活转录因子 BES1 的光介导稳定性。
影响因子：
11.8
作者：
Yang M;Li C;Cai Z;Hu Y;Nolan T;Yu F;Yin Y;Xie Q;Tang G;Wang X
通讯作者：
Wang X
DOI：
10.1111/tpj.12423
发表时间：
2014-03
期刊：
The Plant journal : for cell and molecular biology
影响因子：
--
作者：
Kim B;Jeong YJ;Corvalán C;Fujioka S;Cho S;Park T;Choe S
通讯作者：
Choe S
DOI：
10.1073/pnas.152342599
发表时间：
2002-07-23
影响因子：
11.1
作者：
He, JX;Gendron, JM;Wang, ZY
通讯作者：
Wang, ZY