A Gain-of-Function Mutation in the Arabidopsis Disease Resistance Gene RPP4 Confers Sensitivity to Low Temperature
A Gain-of-Function Mutation in the Arabidopsis Disease Resistance Gene RPP4 Confers Sensitivity to Low Temperature
复制标题
拟南芥抗病基因 RPP4 的功能获得突变赋予低温敏感性
DOI：
10.1104/pp.110.157610
复制
发表时间：
2010-10-01
期刊：
影响因子：
7.4
通讯作者：
Yang, Shuhua
中科院分区：
文献类型：
--
作者：
Huang, Xiaozhen;Li, Jianyong;Yang, Shuhua
植物是如何适应低温的还不是很清楚。为了确定参与低温信号的组件，我们的特点是以前分离的冷敏感2突变体（chs 2）的拟南芥（拟南芥）。该突变体在22 ℃下正常生长，但当温度低于16 ℃时，表现出类似于防御反应激活的表型。这些表型包括叶片发黄和萎蔫、电解质渗漏增加、致病相关基因上调以及过量过氧化氢和水杨酸（SA）积累。此外，chs 2突变体在4 ℃至12 ℃的低温下萌发或转移超过3 d时是幼苗致死的。基于图位的克隆揭示了TIR-NB-LRR（用于Toll/白细胞介素-1受体-核苷酸-结合富含亮氨酸重复序列）-型抗性（R）蛋白RPP 4（用于识别寄生霜霉4）中发生的单个氨基酸取代，其以温度依赖性方式引起R蛋白的失调。chs 2突变导致突变的RPP 4 mRNA转录物增加，防御反应激活，并诱导低温下细胞死亡。此外，chs 2基因内抑制，其中的突变发生在保守的NB结构域，废除防御反应在较低的温度。chs 2与已知SA途径和免疫信号突变体组合的遗传分析表明，chs 2赋予的温度敏感性需要增强的疾病易感性1，这是Mla 12抗性所必需的，并提供skp 1的G2等位基因，但不需要植物毒素缺乏4，PR基因的非表达1或SA。这项研究表明，激活的TIR-NB-LRR蛋白对植物生长和存活的温度敏感性有很大的影响。
How plants adapt to low temperature is not well understood. To identify components involved in low-temperature signaling, we characterized the previously isolated chilling-sensitive2 mutant (chs2) of Arabidopsis (Arabidopsis thaliana). This mutant grew normally at 22 degrees C but showed phenotypes similar to activation of defense responses when shifted to temperatures below 16 degrees C. These phenotypes include yellowish and collapsed leaves, increased electrolyte leakage, up-regulation of PATHOGENESIS RELATED genes, and accumulation of excess hydrogen peroxide and salicylic acid (SA). Moreover, the chs2 mutant was seedling lethal when germinated at or shifted for more than 3 d to low temperatures of 4 degrees C to 12 degrees C. Map-based cloning revealed that a single amino acid substitution occurred in the TIR-NB-LRR (for Toll/Interleukin-1 receptor-nucleotide-binding Leucine-rich repeat)-type resistance (R) protein RPP4 (for Recognition of Peronospora parasitica4), which causes a deregulation of the R protein in a temperature-dependent manner. The chs2 mutation led to an increase in the mutated RPP4 mRNA transcript, activation of defense responses, and an induction of cell death at low temperatures. In addition, a chs2 intragenic suppressor, in which the mutation occurs in the conserved NB domain, abolished defense responses at lower temperatures. Genetic analyses of chs2 in combination with known SA pathway and immune signaling mutants indicate that the chs2-conferred temperature sensitivity requires ENHANCED DISEASE SUSCEPTIBILITY1, REQUIRED FOR Mla12 RESISTANCE, and SUPPRESSOR OF G2 ALLELE OF skp1 but does not require PHYTOALEXIN DEFICIENT4, NONEXPRESSOR OF PR GENES1, or SA. This study reveals that an activated TIR-NB-LRR protein has a large impact on temperature sensitivity in plant growth and survival.