Salicylic acid-independent ENHANCED DISEASE SUSCEPTIBILITY1 signaling in Arabidopsis immunity and cell death is regulated by the monooxygenase FMO1 and the nudix hydrolase NUDT7
Salicylic acid-independent ENHANCED DISEASE SUSCEPTIBILITY1 signaling in Arabidopsis immunity and cell death is regulated by the monooxygenase FMO1 and the nudix hydrolase NUDT7
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DOI：
10.1105/tpc.105.039982
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发表时间：
2006-04-01
期刊：
影响因子：
11.6
通讯作者：
Parker, JE
中科院分区：
文献类型：
--
作者：
Bartsch, M;Gobbato, E;Parker, JE
拟南芥增强的疾病易感性1（EDS 1）控制防御激活和程序性细胞死亡的细胞内Toll相关的免疫受体，识别特定的病原体效应。EDS 1还需要通过限制疾病的进展来对侵入性病原体进行基础抵抗。在这两种反应中，EDS 1在其相互作用伴侣植物抗毒素缺乏症4（PAD 4）的协助下，调节酚类防御分子水杨酸（SA）和其他尚未鉴定的信号中间体的积累。本研究利用拟南芥全基因组芯片技术，通过对拟南芥中两个功能缺失的插入突变体的分析，确定了两个新的免疫调节因子，并对其中两个免疫调节因子的表达依赖于EDS 1和PAD 4的基因进行了鉴定。黄素依赖性单加氧酶1（FMO 1）正调控EDS 1通路，胞质溶质NUDT水解酶家族的一个成员（NUDT 7）负调控EDS 1信号传导。fmo 1和nudt 7突变体单独或与一种严重消耗病原体诱导的SA产生的突变--nudt 2 -1组合的分析指出，在EDS 1条件性疾病抗性和细胞死亡中，FMO 1和NUDT 7具有SA独立功能。相反，我们发现SA拮抗nudt 7突变体中细胞死亡和生长发育迟缓的启动。
Arabidopsis thaliana ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors. EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease. In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and other as yet unidentified signal intermediates. An Arabidopsis whole genome microarray experiment was designed to identify genes whose expression depends on EDS1 and PAD4, irrespective of local SA accumulation, and potential candidates of an SA-independent branch of EDS1 defense were found. We define two new immune regulators through analysis of corresponding Arabidopsis loss-of-function insertion mutants. FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1) positively regulates the EDS1 pathway, and one member (NUDT7) of a family of cytosolic Nudix hydrolases exerts negative control of EDS1 signaling. Analysis of fmo1 and nudt7 mutants alone or in combination with sid2-1, a mutation that severely depletes pathogen-induced SA production, points to SA-independent functions of FMO1 and NUDT7 in EDS1-conditioned disease resistance and cell death. We find instead that SA antagonizes initiation of cell death and stunting of growth in nudt7 mutants.