Dual Role of BKI1 and 14-3-3 s in Brassinosteroid Signaling to Link Receptor with Transcription Factors
Dual Role of BKI1 and 14-3-3 s in Brassinosteroid Signaling to Link Receptor with Transcription Factors
复制标题
DOI：
10.1016/j.devcel.2011.08.018
复制
发表时间：
2011-11-15
影响因子：
11.8
通讯作者：
Wang, Xuelu
中科院分区：
文献类型：
--
作者：
Wang, Haijiao;Yang, Cangjin;Wang, Xuelu
质膜定位的植物类固醇激素受体，油菜素甾醇不敏感1（BRI 1），在没有类固醇的情况下是静止的，主要是由于负调节剂，BRI 1激酶抑制剂1（BKI 1）。在这里，我们报告说，类固醇诱导的，质膜解离和磷酸化的BKI 1也发挥积极的作用，BR信号通过与14-3-3蛋白的子集。BKI 1羧基末端区域的胞质组分增强BR信号传导。该区域中两个丝氨酸残基的突变导致BRI 1激酶的磷酸化减少和组成性质膜定位。14-3-3蛋白可以通过含有两个磷酸化位点的基序与磷酸化的BKI 1相互作用，以释放BKI 1对BRI 1的抑制。同时，胞质BKII拮抗14-3-3 s并增强BRI 1 EMS SUPPLYOR 1（BES 1）/BRASSINAZOLE RESISTANT 1（BZR 1）在细胞核中的积累以调节BR反应。
The plasma membrane-localized plant steroid hormone receptor, BRASSINOSTEROID INSENSITIVE 1 (BRI1), is quiescent in the absence of steroids, largely due to a negative regulator, BRI1 KINASE INHIBITOR 1 (BKI1). Here, we report that the steroid-induced, plasma membrane-dissociated and phosphorylated BKI1 also plays positive roles in BR signaling by interacting with a subset of 14-3-3 proteins. The cytosolic fraction of BKI1 carboxyl terminal region enhances BR signaling. Mutations of two serine residues in this region lead to reduced phosphorylation by the BRI1 kinase and constitutive plasma membrane localization. The 14-3-3 proteins can interact with the phosphorylated BKIl through a motif that contains the two phosphorylation sites to release inhibition of BRI1 by BKI1. Meanwhile, the cytosolic BKIl antagonizes the 14-3-3 s and enhances accumulation of BRI1 EMS SUPPRESSOR 1 (BES1)/BRASSINAZOLE RESISTANT 1 (BZR1) in the nucleus to regulate BR-responses.