The CAPE1 peptide confers resistance against bacterial wilt in tomato.

IF 5.7 2区 生物学 Q1 PLANT SCIENCES
Weiqi Zhang, Marc Planas-Marquès, Moyan Liang, Qingshan Zhang, Annemarie Vermeulen, Farnusch Kaschani, Markus Kaiser, Frank L W Takken, Nuria S Coll, Marc Valls
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Abstract

Bacterial wilt caused by Ralstonia solanacearum is one of the most destructive bacterial diseases for which no effective treatment exists. There is an urgent need to understand the basis of resistance against this pathogen in order to engineer efficient strategies in the field. We previously demonstrated that resistant tomato plants limit bacterial movement in the apoplast and the xylem. As a first step to dissect the underlying mechanisms, we analysed the apoplast proteome upon challenge with R. solanacearum in the susceptible tomato cultivar Marmande and the resistant cultivar Hawaii 7996. Here, we described the xylem proteome in these same cultivars and compared it with the apoplastic proteome, revealing variety-dependent and infection-dependent changes. This proteomic analysis led to the identification of pathogenesis-related 1 (PR1) proteins as highly induced upon infection. Since PR1b was the most abundant PR1 protein in both the apoplast and the xylem, we concentrated on this family member to study the role of PR1s in the interaction between tomato and R. solanacearum. Surprisingly, lack of PR1b resulted in enhanced resistance to R. solanacearum in tomato, which could be due to an up-regulation of homologous genes in a compensatory effect as has been reported before. PR1 processing by an unknown protease in tomato results in the generation of the CAPE peptide. Treatment of tomato plants with the CAPE1 peptide resulted in restriction of R. solanacearum growth, via defence gene reprogramming. Future work in the lab will help determine which tomato secreted proteases cleave PR1s to generate CAPEs.

CAPE1 肽能增强番茄对细菌性枯萎病的抗性。
青枯病(Ralstonia solanacearum)是一种最具破坏性的细菌性病害,目前尚无有效的治疗方法。迫切需要了解对这种病原体的耐药性基础,以便在该领域设计有效的策略。我们之前证明了抗性番茄植物限制了外质体和木质部的细菌运动。作为剖析其潜在机制的第一步,我们分析了番茄易感品种Marmande和抗病品种夏威夷7996受番茄红枯病菌侵染后的外质体蛋白质组。在这里,我们描述了这些相同品种的木质部蛋白质组,并将其与外质体蛋白质组进行了比较,揭示了品种依赖性和感染依赖性的变化。这种蛋白质组学分析导致PR1s在感染后被高度诱导。由于PR1b是外质体和木质部中含量最多的PR1蛋白,因此我们以该家族成员为研究对象,研究PR1s在番茄与番茄红霉相互作用中的作用。令人惊讶的是,缺乏PR1b导致番茄对番茄红霉的抗性增强,这可能是由于同源基因在补偿作用中的上调,正如之前报道的那样。在番茄中,一种未知的蛋白酶对PR1的处理导致了CAPE肽的产生。用CAPE1肽处理番茄植株,通过防御基因重编程,导致番茄红霉生长受限。实验室未来的工作将有助于确定哪些番茄分泌蛋白酶裂解pr1以产生CAPEs。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Experimental Botany
Journal of Experimental Botany 生物-植物科学
CiteScore
12.30
自引率
4.30%
发文量
450
审稿时长
1.9 months
期刊介绍: The Journal of Experimental Botany publishes high-quality primary research and review papers in the plant sciences. These papers cover a range of disciplines from molecular and cellular physiology and biochemistry through whole plant physiology to community physiology. Full-length primary papers should contribute to our understanding of how plants develop and function, and should provide new insights into biological processes. The journal will not publish purely descriptive papers or papers that report a well-known process in a species in which the process has not been identified previously. Articles should be concise and generally limited to 10 printed pages.
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