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
复制标题
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
复制
发表时间:
2010-07-01
期刊:
影响因子:
7.2
通讯作者:
Yang, Shuhua
中科院分区:
文献类型:
--
作者:
Yang, Haibian;Shi, Yiting;Yang, Shuhua
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.