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The Proteomics of Resistance to Halo Blight in Common Bean.
Molecular Plant-Microbe Interactions ( IF 3.5 ) Pub Date : 2020-07-29 , DOI: 10.1094/mpmi-05-20-0112-r
Bret Cooper 1 , Kimberly B Campbell 1 , Hunter S Beard 1 , Wesley M Garrett 2 , Marcio E Ferreira 3, 4
Affiliation  

Halo blight disease of beans is caused by a gram-negative bacterium, Pseudomonas syringae pv. phaseolicola. The disease is prevalent in South America and Africa and causes crop loss for indigent people who rely on beans as a primary source of daily nutrition. In susceptible beans, P. syringae pv. phaseolicola causes water-soaking at the site of infection and produces phaseolotoxin, an inhibitor of bean arginine biosynthesis. In resistant beans, P. syringae pv. phaseolicola triggers a hypersensitive response that limits the spread of infection. Here, we used high-throughput mass spectrometry to interrogate the responses to two different P. syringae pv. phaseolicola isolates on a single line of common bean, Phaseolus vulgaris PI G19833, with a reference genome sequence. We obtained quantitative information for 4,135 bean proteins. A subset of 160 proteins with similar accumulation changes during both susceptible and resistant reactions included salicylic acid responders EDS1 and NDR1, ethylene and jasmonic acid biosynthesis enzymes, and proteins enabling vesicle secretion. These proteins revealed the activation of a basal defense involving hormonal responses and the mobilization of extracellular proteins. A subset of 29 proteins specific to hypersensitive immunity included SOBIR1, a G-type lectin receptor–like kinase, and enzymes needed for glucoside and phytoalexin production. Virus-induced gene silencing revealed that the G-type lectin receptor–like kinase suppresses bacterial infection. Together, the results define the proteomics of disease resistance to P. syringae pv. phaseolicola in beans and support a model whereby the induction of hypersensitive immunity reinstates defenses targeted by P. syringae pv. phaseolicola.



中文翻译:

普通豆抗光晕病的蛋白质组学。

豆类的枯萎病是由革兰氏阴性细菌丁香假单胞菌pv引起的。菜豆。该病在南美和非洲很普遍,对依赖豆类作为日常营养主要来源的贫困人口造成作物歉收。在易感豆中,丁香假单胞菌PV。菜豆在感染位点浸水并产生菜豆毒素,豆精氨酸生物合成抑制剂。在抗性豆中,丁香假单胞菌PV。菜豆草触发超敏反应,限制了感染的传播。在这里,我们使用高通量质谱法来询问对两种不同丁香假单胞菌PV的反应。菜豆株上菜豆的单线,菜豆PI G19833,具有参考基因组序列。我们获得了4,135种豆类蛋白质的定量信息。在易感和耐药反应期间具有相似积累变化的160种蛋白质的子集包括水杨酸应答剂EDS1和NDR1,乙烯和茉莉酸生物合成酶,以及使囊泡分泌的蛋白质。这些蛋白揭示了涉及激素反应的基础防御的激活和细胞外蛋白的动员。特异于超敏免疫的29种蛋白质的子集包括SOBIR1,一种G型凝集素受体样激酶,以及产生糖苷和植物抗毒素的酶。病毒引起的基因沉默表明,G型凝集素受体样激酶可抑制细菌感染。在一起,结果定义了蛋白质组学对疾病的抵抗力丁香假单胞菌PV。豆中的菜豆,并支持一种模型,通过该模型,超敏免疫的诱导可恢复丁香假单胞菌pv靶向的防御。菜豆

更新日期:2020-08-28
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