A mutant CHS3 protein with TIR-NB-LRR-LIM domains modulates growth, cell death and freezing tolerance in a temperature-dependent manner in Arabidopsis

A mutant CHS3 protein with TIR-NB-LRR-LIM domains modulates growth, cell death and freezing tolerance in a temperature-dependent manner in Arabidopsis
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具有 TIR-NB-LRR-LIM 结构域的突变 CHS3 蛋白以温度依赖性方式调节拟南芥的生长、细胞死亡和冷冻耐受性

DOI:
10.1111/j.1365-313x.2010.04241.x
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发表时间:
2010-07-01
期刊:
影响因子:
7.2
通讯作者:
Yang, Shuhua
Yang, Shuhua
中科院分区:
生物学1区
文献类型:
--
作者:
Yang, Haibian;Shi, Yiting;Yang, Shuhua

文献摘要

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低温是限制植物生长平衡和植物与病原菌互作的环境因子之一。最近的研究表明,温度反应和防御反应之间的联系,但是,潜在的分子机制仍然不清楚。本研究对拟南芥中的冷敏感突变体chs 3 -1进行了研究。chs 3 -1植物在16 ℃生长或从22 ℃转移到4 ℃时表现出生长停滞和失绿。chs 3 -1植物在16 ℃下也表现出组成型激活的防御反应,其在较高温度(22 ℃)下减轻。基于图位克隆的CHS 3揭示了它编码属于TIR-NB-LRR类的非常规抗病(R)蛋白,在羧基末端具有锌结合LIM结构域(Lin-11、Isl-1和Mec-3结构域)。保守的含LIM结构域中的chs 3 -1突变导致TIR-NB-LRR结构域的组成性激活。结果表明,eds 1、sgt 1b和rar 1完全抑制chs 3 -1的生长和防御表型,pad 4和nahG部分抑制chs 3 -1的生长和防御表型,而npr 1和ndr 1不抑制chs 3 -1的生长和防御表型。有趣的是,在16摄氏度下生长的chs 3 -1植物对冷冻温度的耐受性增强。这种耐受性与由激活的防御反应引起的生长缺陷和细胞死亡表型相关。其他具有激活防御反应的突变体,包括cpr 1,cpr 5和slh 1也显示出增强的抗冻性。这些发现揭示了一个非传统的突变体R基因在植物生长、防御反应和冷胁迫中的作用,表明冷信号和防御反应之间存在相互作用。
P>Low temperature is one of environmental factors that restrict plant growth homeostasis and plant-pathogen interactions. Recent studies suggest a link between temperature responses and defense responses; however, the underlying molecular mechanisms remain unclear. In this study, the chilling sensitive 3 (chs3-1) mutant in Arabidopsis was characterized. chs3-1 plants showed arrested growth and chlorosis when grown at 16 degrees C or when shifted from 22 to 4 degrees C. chs3-1 plants also exhibited constitutively activated defense responses at 16 degrees C, which were alleviated at a higher temperature (22 degrees C). Map-based cloning of CHS3 revealed that it encodes an unconventional disease resistance (R) protein belonging to the TIR-NB-LRR class with a zinc-binding LIM domain (Lin-11, Isl-1 and Mec-3 domains) at the carboxyl terminus. The chs3-1 mutation in the conserved LIM-containing domain led to the constitutive activation of the TIR-NB-LRR domain. Consistently, the growth and defense phenotypes of chs3-1 plants were completely suppressed by eds1, sgt1b and rar1, partially by pad4 and nahG, but not by npr1 and ndr1. Intriguingly, chs3-1 plants grown at 16 degrees C showed enhanced tolerance to freezing temperatures. This tolerance was correlated with growth defect and cell death phenotypes caused by activated defense responses. Other mutants with activated defense responses, including cpr1, cpr5 and slh1 also displayed enhanced freezing tolerance. These findings revealed a role of an unconventional mutant R gene in plant growth, defense response and cold stress, suggesting a mutual interaction between cold signaling and defense responses.