Nuclear-localized BZR1 mediates brassinosteroid-induced growth and feedback suppression of brassinosteroid biosynthesis

被引：926

作者：

Wang, ZY

Nakano, T

Gendron, J

He, JX

Chen, M

Vafeados, D

Yang, YL

Fujioka, S

Yoshida, S

Asami, T

Chory, J

机构：

[1] Salk Inst Biol Studies, Howard Hughes Med Inst, La Jolla, CA 92037 USA

[2] Salk Inst Biol Studies, Plant Biol Lab, La Jolla, CA 92037 USA

[3] Carnegie Inst Washington, Dept Plant Biol, Stanford, CA 94305 USA

[4] Inst Phys & Chem Res, Plant Funct Lab, Wako, Saitama 3510198, Japan

来源：

DEVELOPMENTAL CELL | 2002年 / 2卷 / 04期

基金：

美国国家科学基金会;

关键词：

D O I：

10.1016/S1534-5807(02)00153-3

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Plant steroid hormones, brassinosteroids (BRs), are perceived by a cell surface receptor kinase, BRI1, but how BR binding leads to regulation of gene expression in the nucleus is unknown. Here we describe the identification of BZR1 as a nuclear component of the BR signal transduction pathway. A dominant mutation bzr1-1D suppresses BR-deficient and BR-insensitive (bri1) phenotypes and enhances feedback inhibition of BR biosynthesis. BZR1 protein accumulates in the nucleus of elongating cells of dark-grown hypocotyls and is stabilized by BR signaling and the bzr1-1D mutation. Our results demonstrate that BZR1 is a positive regulator of the BR signaling pathway that mediates both downstream BR responses and feedback regulation of BR biosynthesis.

引用

页码：505 / 513

页数：9