Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine-insensitive (coi1) mutation occurs through two distinct mechanisms
Resistance to Pseudomonas syringae conferred by an Arabidopsis thaliana coronatine-insensitive (coi1) mutation occurs through two distinct mechanisms
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DOI：
10.1046/j.1365-313x.2001.01050.x
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发表时间：
2001-06-01
期刊：
影响因子：
7.2
通讯作者：
Kunkel, BN
中科院分区：
文献类型：
--
作者：
Kloek, AP;Verbsky, ML;Kunkel, BN
一个新的等位基因的冠菌素不敏感的基因座（COI 1）中分离出的拟南芥突变体的细菌病原体假单胞菌的抗性增强的屏幕。这种突变体，命名为coi 1 -20，表现出强大的抗几个P. erichingae分离物，但仍然敏感的致病菌Erisyphe和花椰菜花叶病毒。coi 1 -20植物对丁香假单胞菌菌株PstDC 3000的抗性与感染后PR-1表达的过度激活和水杨酸（SA）水平升高的积累相关，这表明SA介导的防御反应途径在该突变体中被致敏。PstDC 3000在coi 1 -20叶片中的生长限制部分依赖于NPR 1，完全依赖于SA，表明SA介导的防御是限制PstDC 3000在coi 1 -20植物中生长所必需的。令人惊讶的是，尽管在携带水杨酸羟化酶（nahG）转基因的coil 1 -20植物中PsdDC 3000生长水平高，但这些植物不表现出疾病症状。因此，在coil 1 -20植物中对P. erichingae的抗性由两种不同的机制赋予：（i）通过激活SA依赖性防御途径限制病原体生长;和（ii）不依赖于SA的不能发展疾病症状。这些发现与以下假设一致，即P. dichloringae植物毒素冠菌素通过抑制宿主防御反应和促进病变形成来促进毒力。
A new allele of the coronatine-insensitive locus (COI1) was isolated in a screen for Arabidopsis thaliana mutants with enhanced resistance to the bacterial pathogen Pseudomonas syringae. This mutant, designated coi1-20, exhibits robust resistance to several P. syringae isolates but remains susceptible to the virulent pathogens Erisyphe and cauliflower mosaic virus. Resistance to P. syringae strain PstDC3000 in coi1-20 plants is correlated with hyperactivation of PR-1 expression and accumulation of elevated levels of salicylic acid (SA) following infection, suggesting that the SA-mediated defense response pathway is sensitized in this mutant. Restriction of growth of PstDC3000 in coi1-20 leaves is partially dependent on NPR1 and fully dependent on SA, indicating that SA-mediated defenses are required for restriction of PstDC3000 growth in coi1-20 plants. Surprisingly, despite high levels of PsdDC3000 growth in coi1-20 plants carrying the salicylate hydroxylase (nahG) transgene, these plants do not exhibit disease symptoms. Thus resistance to P. syringae in coi1-20 plants is conferred by two different mechanisms: (i) restriction of pathogen growth via activation of the SA-dependent defense pathway; and (ii) an SA-independent inability to develop disease symptoms. These findings are consistent with the hypotheses that the P. syringae phytotoxin coronatine acts to promote virulence by inhibiting host defense responses and by promoting lesion formation.