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首页> 外文期刊>Molecules and cells >Priming by Rhizobacterium Protects Tomato Plants from Biotrophic and Necrotrophic Pathogen Infections through Multiple Defense Mechanisms
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Priming by Rhizobacterium Protects Tomato Plants from Biotrophic and Necrotrophic Pathogen Infections through Multiple Defense Mechanisms

机译:根瘤菌的启动通过多种防御机制保护番茄植物免受营养和坏死性病原体的感染

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A selected strain of rhizobacterium, Pseudomonas putida strain LSW17S (LSW17S), protects tomato plants (Lyco-persicon esculentum L. cv. Seokwang) from bacterial speck by biotrophic Pseudomonas syringae pv. tomato strain DC3000 (DC3000) and bacterial wilt by necrotrophic Ralstonia solanacearum KACC 10703 (Rs10703). To investigate defense mechanisms induced by LSW17S in tomato plants, transcription patterns of pathogenesis-related (PR) genes and H 2 O 2 production were analyzed in plants treated with LSW17S and subsequent pathogen inoculation. LSW17S alone did not induce transcriptions of employed PR genes in leaves and roots. DC3000 challenge following LSW17S triggered rapid transcriptions of PR genes and H 2 O 2 production in leaves and roots. Catalase infiltration with DC3000 attenuated defense-related responses and resistance against DC3000 infection. Despite depriving H 2 O 2 production and PR1b transcription by the same treatment, resistance against Rs10703 infection was not deterred significantly. H 2 O 2 is indispensable for defense signaling and/or mechanisms primed by LSW17S and inhibition of bacterial speck, however, it is not involved in resistance against bacterial wilt.
机译:选定的根瘤菌菌株恶臭假单胞菌菌株LSW17S(LSW17S)通过生物营养型丁香假单胞菌pv保护番茄植物(Lyco-persicon esculentum L. cv。Seokwang)免受细菌斑点侵害。番茄菌株DC3000(DC3000)和坏死性青枯雷尔氏菌KACC 10703(Rs10703)使细菌枯萎。为了研究LSW17S诱导的番茄防御机制,分析了用LSW17S处理并随后接种病原体的病原相关(PR)基因的转录模式和H 2 O 2的产生。单独的LSW17S不会诱导叶和根中所用PR基因的转录。 LSW17S引发的DC3000攻击触发了叶和根中PR基因的快速转录和H 2 O 2的产生。带有DC3000的过氧化氢酶浸润减弱了防御相关反应和对DC3000感染的抵抗力。尽管通过相同的处理剥夺了H 2 O 2的产生和PR1b的转录,但对Rs10703感染的抗性并未得到显着抑制。 H 2 O 2对于由LSW17S启动的防御信号和/或机制以及对细菌斑点的抑制是必不可少的,但是,它不涉及对青枯病的抗性。

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