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一种细菌效应蛋白揭示了植物代谢途径参与耐受细菌性萎蔫病。

A bacterial effector protein uncovers a plant metabolic pathway involved in tolerance to bacterial wilt disease.

机构信息

Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences; Chinese Academy of Sciences, Shanghai 201602, China; University of Chinese Academy of Sciences, Beijing, China.

Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences; Chinese Academy of Sciences, Shanghai 201602, China.

出版信息

Mol Plant. 2021 Aug 2;14(8):1281-1296. doi: 10.1016/j.molp.2021.04.014. Epub 2021 May 1.

Abstract

Bacterial wilt caused by the soil-borne plant pathogen Ralstonia solanacearum is a devastating disease worldwide. Upon plant colonization, R. solanacearum replicates massively, causing plant wilting and death; collapsed infected tissues then serve as a source of inoculum. In this work, we show that the plant metabolic pathway mediated by pyruvate decarboxylases (PDCs) contributes to plant tolerance to bacterial wilt disease. Arabidopsis and tomato plants respond to R. solanacearum infection by increasing PDC activity, and plants with deficient PDC activity are more susceptible to bacterial wilt. Treatment with either pyruvic acid or acetic acid (substrate and product of the PDC pathway, respectively) enhances plant tolerance to bacterial wilt disease. An effector protein secreted by R. solanacearum, RipAK, interacts with PDCs and inhibits their oligomerization and enzymatic activity. Collectively, our work reveals a metabolic pathway involved in plant resistance to biotic and abiotic stresses, and a bacterial virulence strategy to promote disease and the completion of the pathogenic life cycle.

摘要

由土壤植物病原体罗尔斯顿氏菌引起的细菌性萎蔫病是一种全球性的破坏性疾病。在植物定殖后,罗尔斯顿氏菌大量复制,导致植物萎蔫和死亡;随后崩溃的感染组织成为接种物的来源。在这项工作中,我们表明,由丙酮酸脱羧酶(PDC)介导的植物代谢途径有助于植物对细菌性萎蔫病的耐受性。拟南芥和番茄植物对罗尔斯顿氏菌感染的反应是增加 PDC 活性,而 PDC 活性缺陷的植物更容易感染细菌性萎蔫病。用丙酮酸或乙酸(PDC 途径的底物和产物)处理可增强植物对细菌性萎蔫病的耐受性。罗尔斯顿氏菌分泌的一种效应蛋白 RipAK 与 PDC 相互作用,抑制其寡聚化和酶活性。总之,我们的工作揭示了参与植物对生物和非生物胁迫的抗性的代谢途径,以及促进疾病和完成致病生命周期的细菌毒力策略。

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