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UV-B诱导的UVR8光感受器核积累需要COP1。

COP1 is required for UV-B-induced nuclear accumulation of the UVR8 photoreceptor.

作者信息

Yin Ruohe, Skvortsova Mariya Y, Loubéry Sylvain, Ulm Roman

机构信息

Department of Botany and Plant Biology, University of Geneva, CH-1211 Geneva 4, Switzerland;

Department of Botany and Plant Biology, University of Geneva, CH-1211 Geneva 4, Switzerland; Institute of Genetics and Genomics of Geneva, University of Geneva, CH-1211 Geneva 4, Switzerland

出版信息

Proc Natl Acad Sci U S A. 2016 Jul 26;113(30):E4415-22. doi: 10.1073/pnas.1607074113. Epub 2016 Jul 12.

DOI:10.1073/pnas.1607074113
PMID:27407149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4968759/
Abstract

The UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8) promotes UV-B acclimation and tolerance in Arabidopsis thaliana UVR8 localizes to both cytosol and nucleus, but its main activity is assumed to be nuclear. UV-B photoreception stimulates nuclear accumulation of UVR8 in a presently unknown manner. Here, we show that CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1) is required for UV-B-induced nuclear accumulation of UVR8, but bypassing the COP1 requirement for UVR8 nuclear accumulation did not rescue the cop1 mutant UV-B phenotype. Using a glucocorticoid receptor (GR)-based fusion protein system to conditionally localize GR-UVR8 to the nucleus, we have demonstrated that both photoactivation and nuclear localization of UVR8 are required for UV-B-induced photomorphogenic responses. In contrast, there was no UV-B response when UV-B-activated UVR8 was artificially retained in the cytosol. In agreement with a predominantly nuclear activity, constitutively active UVR8(W285A) accumulated in the nucleus also in the absence of UV-B. Furthermore, GR-COP1 expression lines suggested that UV-B-activated UVR8 can be coimported into the nucleus by COP1. Our data strongly support localization of UVR8 signaling in the nucleus and a dual role for COP1 in the regulation of UV-B-induced UVR8 nuclear accumulation and in UVR8-mediated UV-B signaling.

摘要

紫外线B光感受器紫外线抗性位点8(UVR8)促进拟南芥对紫外线B的适应性和耐受性。UVR8定位于细胞质和细胞核,但推测其主要活性位于细胞核。紫外线B光感受以目前未知的方式刺激UVR8在细胞核中的积累。在这里,我们表明组成型光形态建成1(COP1)是紫外线B诱导的UVR8细胞核积累所必需的,但绕过COP1对UVR8细胞核积累的需求并不能挽救cop1突变体的紫外线B表型。使用基于糖皮质激素受体(GR)的融合蛋白系统将GR-UVR8条件性地定位于细胞核,我们证明UVR8的光激活和细胞核定位都是紫外线B诱导的光形态建成反应所必需的。相比之下,当紫外线B激活的UVR8被人为地保留在细胞质中时,没有紫外线B反应。与主要在细胞核中的活性一致,组成型活性UVR8(W285A)在没有紫外线B的情况下也在细胞核中积累。此外,GR-COP1表达系表明紫外线B激活的UVR8可以被COP1共同导入细胞核。我们的数据有力地支持了UVR8信号在细胞核中的定位以及COP1在调节紫外线B诱导的UVR8细胞核积累和UVR8介导的紫外线B信号传导中的双重作用。

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本文引用的文献

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