Gupta V, Willits M G, Glazebrook J
Molecular and Cell Biology Graduate Program, University of Maryland, College Park 20742, USA.
Mol Plant Microbe Interact. 2000 May;13(5):503-11. doi: 10.1094/MPMI.2000.13.5.503.
The Arabidopsis enhanced disease susceptibility 4 (eds4) mutation causes enhanced susceptibility to infection by the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326). Gene-for-gene resistance to bacteria carrying the avirulence gene avrRpt2 is not significantly affected by eds4. Plants homozygous for eds4 exhibit reduced expression of the pathogenesis-related gene PR-1 after infection by Psm ES4326, weakened responses to treatment with the signal molecule salicylic acid (SA), impairment of the systemic acquired resistance response, and reduced accumulation of SA after infection with Psm ES4326. These phenotypes indicate that EDS4 plays a role in SA-dependent signaling. SA has been shown to have a negative effect on activation of gene expression by the signal molecule jasmonic acid (JA). Two mutations that cause reduced SA levels, eds4 and pad4, cause heightened responses to inducers of JA-dependent gene expression, providing genetic evidence to support the idea that SA interferes with JA-dependent signaling. Two possible working models of the role of EDS4 in governing activation of defense responses are presented.
拟南芥增强病害易感性4（eds4）突变导致对细菌病原体丁香假单胞菌番茄致病变种ES4326（Psm ES4326）感染的易感性增强。对携带无毒基因avrRpt2的细菌的基因对基因抗性不受eds4的显著影响。eds4纯合的植物在被Psm ES4326感染后，病程相关基因PR-1的表达降低，对信号分子水杨酸（SA）处理的反应减弱，系统获得性抗性反应受损，并且在被Psm ES4326感染后SA的积累减少。这些表型表明EDS4在SA依赖的信号传导中起作用。已表明SA对信号分子茉莉酸（JA）激活基因表达有负面影响。导致SA水平降低的两个突变体eds4和pad4，对JA依赖的基因表达诱导剂的反应增强，提供了遗传证据支持SA干扰JA依赖的信号传导这一观点。本文提出了EDS4在调控防御反应激活中作用的两种可能工作模型。
