Abscisic Acid Deficiency Antagonizes High-Temperature Inhibition of Disease Resistance through Enhancing Nuclear Accumulation of Resistance Proteins SNC1 and RPS4 in Arabidopsis
Abscisic Acid Deficiency Antagonizes High-Temperature Inhibition of Disease Resistance through Enhancing Nuclear Accumulation of Resistance Proteins SNC1 and RPS4 in Arabidopsis
复制标题
拟南芥脱落酸缺乏通过增强抗性蛋白SNC1和RPS4的核积累来拮抗高温抑制抗病性
DOI：
10.1105/tpc.112.096198
复制
发表时间：
2012-03-01
期刊：
影响因子：
11.6
通讯作者：
Hua, Jian
中科院分区：
文献类型：
--
作者：
Mang, Hyung-Gon;Qian, Weiqiang;Hua, Jian
植物对病原体的防御反应受非生物因素的影响，包括温度。高温通常会抑制抗病蛋白的活性及其介导的防御反应。利用拟南芥温度敏感性自身免疫突变体bonzai 1进行的突变体筛选显示，脱落酸（阿坝）缺陷型突变体aba 2增强了由抗性（R）基因SUPPLYOR OF npr 1 -1 CONSTITUTIVE 1（SNC 1）介导的高温抗性。阿坝缺乏促进SNC 1的核积累，这是它在低温和高温下发挥作用所必需的。此外，阿坝缺乏对SNC 1蛋白积累的影响是独立的水杨酸，其作用往往被阿坝拮抗。阿坝缺乏还促进了高温下抗丁香假单胞菌R蛋白的活性和核定位，表明阿坝对R蛋白定位和核活性的影响是广泛的。相比之下，突变，赋予阿坝不敏感性没有促进防御反应，在高温下，这表明无论是组织特异性的阿坝信号或ABA的作用，在防御调节独立的核心阿坝信号机制。综上所述，本研究揭示了阿坝和抗病性之间通过R蛋白定位的一个新的交叉点，并提供了非生物和生物反应之间的拮抗作用的进一步证据。
Plant defense responses to pathogens are influenced by abiotic factors, including temperature. Elevated temperatures often inhibit the activities of disease resistance proteins and the defense responses they mediate. A mutant screen with an Arabidopsis thaliana temperature-sensitive autoimmune mutant bonzai1 revealed that the abscisic acid (ABA)-deficient mutant aba2 enhances resistance mediated by the resistance (R) gene SUPPRESSOR OF npr1-1 CONSTITUTIVE1 (SNC1) at high temperature. ABA deficiency promoted nuclear accumulation of SNC1, which was essential for it to function at low and high temperatures. Furthermore, the effect of ABA deficiency on SNC1 protein accumulation is independent of salicylic acid, whose effects are often antagonized by ABA. ABA deficiency also promotes the activity and nuclear localization of R protein RESISTANCE TO PSEUDOMONAS SYRINGAE4 at higher temperature, suggesting that the effect of ABA on R protein localization and nuclear activity is rather broad. By contrast, mutations that confer ABA insensitivity did not promote defense responses at high temperature, suggesting either tissue specificity of ABA signaling or a role of ABA in defense regulation independent of the core ABA signaling machinery. Taken together, this study reveals a new intersection between ABA and disease resistance through R protein localization and provides further evidence of antagonism between abiotic and biotic responses.