Arabidopsis STO/BBX24 negatively regulates UV-B signaling by interacting with COP1 and repressing HY5 transcriptional activity
Arabidopsis STO/BBX24 negatively regulates UV-B signaling by interacting with COP1 and repressing HY5 transcriptional activity
复制标题
拟南芥 STO/BBX24 通过与 COP1 相互作用并抑制 HY5 转录活性来负调节 UV-B 信号传导
DOI：
10.1038/cr.2012.34
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发表时间：
2012-06-01
期刊：
影响因子：
44.1
通讯作者：
Li, Shao-Shan
中科院分区：
文献类型：
--
作者：
Jiang, Lei;Wang, Yan;Li, Shao-Shan
UV-B （280-315 nm）是太阳辐射的一个组成部分，可以作为胁迫诱导剂或发育信号。近年来，人们越来越关注低通量uv - b诱导的光形态发生反应，并确定了该反应的几个关键参与者，包括UVR8（一种uv - b特异性光受体）、COP1（一种含有wd40 -重复的环指蛋白）、HY5（一种基本拉链转录因子）和RUP1/2（两种UVR8相互作用蛋白）。在这里，我们报道了拟南芥耐盐性（STO/BBX24），一个已知的植物光信号调节因子，在uv - b介导的光形态发生中定义了一个新的信号成分。bbx24突变体对UV-B辐射极度敏感，在UV-B处理下变得极度矮小。相比之下，BBX24过表达转基因品系对UV-B的反应要比BBX24和野生型植株弱得多。BBX24的表达是由UV-B诱导的，其在UV-B下的积累需要COP1。共免疫沉淀实验表明，在UV-B照射下，植物中BBX24与COP1相互作用。此外，BBX24与HY5相互作用，并与HY5拮抗uv - b诱导的下胚轴伸长抑制。此外，BBX24可减弱uv - b诱导的HY5积累并抑制其转录激活活性。综上所述，我们的研究结果揭示了光调节BBX24在UV-B反应中的一个以前未被表征的功能，并证明BBX24通过与COP1和HY5相互作用，作为光形态发生UV-B反应的负调节因子。UV-B诱导的表达模式及其对HY5活性的抑制表明，BBX24可能是植物中UV-B信号反馈调控模块的新组成部分。
UV-B (280-315 nm) is an integral part of solar radiation and can act either as a stress inducer or as a developmental signal. In recent years, increasing attention has been paid to the low-fluence UV-B-induced photomorphogenic response and several key players in this response have been identified, which include UVR8 (a UV-B-specific photoreceptor), COP1 (a WD40-repeat-containing RING finger protein), HY5 (a basic zipper transcription factor), and RUP1/2 (two UVR8-interacting proteins). Here we report that Arabidopsis SALT TOLERANCE (STO/BBX24), a known regulator for light signaling in plants, defines a new signaling component in UV-B-mediated photomorphogenesis. The bbx24 mutant is hypersensitive to UV-B radiation and becomes extremely dwarfed under UV-B treatment. By contrast, BBX24 overexpression transgenic lines respond much more weakly to UV-B than the bbx24 and wild-type plants. BBX24 expression is UV-B-inducible and its accumulation under UV-B requires COP1. Co-immunoprecipitation experiments indicate that BBX24 interacts with COP1 in planta upon UV-B illumination. Moreover, BBX24 interacts with HY5 and acts antagonistically with HY5 in UV-B-induced inhibition of hypocotyl elongation. Furthermore, BBX24 attenuates UV-B-induced HY5 accumulation and suppresses its transcription-activation activity. Taken together, our results reveal a previously uncharacterized function of the light-regulated BBX24 in UV-B responses and demonstrate that BBX24 functions as a negative regulator of photomorphogenic UV-B responses by interacting with both COP1 and HY5. The UV-B-inducible expression pattern and its suppression of HY5 activity suggest that BBX24 could be a new component of the feedback regulatory module of UV-B signaling in plants.