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由黄单胞菌属细菌引起的多叶性虫瘿病。

The leafy gall syndrome induced by Rhodococcus fascians.

机构信息

Department of Plant Biotechnology and Bioinformatics, Ghent University, Gent, Belgium.

出版信息

FEMS Microbiol Lett. 2013 May;342(2):187-94. doi: 10.1111/1574-6968.12119. Epub 2013 Apr 2.

Abstract

The Actinomycete Rhodococcus fascians causes the leafy gall syndrome, an infectious plant disease that affects a wide range of plants, primarily dicotyledonous herbs. The syndrome is associated with delayed senescence, loss of apical dominance, activation of dormant axillary meristems, and formation of multiple inflorescences, leading to a stunted and bushy plant appearance. A major breakthrough in the elucidation of the virulence strategy of this pathogen was the discovery of a linear virulence plasmid, pFiD188 for R. fascians strain D188. Upon perception of a compatible host plant, an autoregulatory mechanism mediated by the att operon directs a switch in the bacterial life style from a harmless epiphyte into a pathogenic endophyte and, concomitantly, activates gene expression of the fas operon that encodes a cytokinin biosynthesis pathway. A mixture of five cytokinins determines the cytokinin activity of R. fascians that directly affects plant responses and development. Moreover, the bacterial cytokinins stimulate the host to produce auxins and polyamines, that function as accessory signals to aid in symptom development. The plant reacts against the developmental hijacking by R. fascians by activating a set of counteracting measures that ultimately results in a delicate balance, allowing a long-lasting biotrophic interaction.

摘要

放线菌 Rhodococcus fascians 引起叶状瘤综合征,这是一种传染性植物疾病,影响范围广泛的植物,主要是双子叶草本植物。该综合征与衰老延迟、顶端优势丧失、休眠腋芽分生组织的激活以及多个花序的形成有关,导致植物矮小丛生。阐明该病原体毒力策略的一个重大突破是发现了线性毒力质粒 pFiD188 用于 R. fascians 菌株 D188。一旦感知到相容的宿主植物,由 att 操纵子介导的自动调节机制将细菌的生活方式从无害的附生菌转变为致病的内生菌,并同时激活 fas 操纵子的基因表达,该操纵子编码细胞分裂素生物合成途径。五种细胞分裂素的混合物决定了 R. fascians 的细胞分裂素活性,直接影响植物的反应和发育。此外,细菌细胞分裂素刺激宿主产生生长素和多胺,作为辅助信号以帮助症状的发展。植物通过激活一系列对抗措施来对抗 R. fascians 的发育劫持,最终导致微妙的平衡,允许长期的生物营养相互作用。

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