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SseF,一种来自哺乳动物病原体沙门氏菌的 III 型效应蛋白,需要抗性基因介导的信号来激活模式植物烟草原生质体的细胞死亡。

SseF, a type III effector protein from the mammalian pathogen Salmonella enterica, requires resistance-gene-mediated signalling to activate cell death in the model plant Nicotiana benthamiana.

机构信息

Department Biologie, Lehrstuhl für Biochemie, Friedrich Alexander Universität Erlangen-Nürnberg, Staudtstr. 5, 91058 Erlangen, Germany.

Infektionsbiologische Abteilung im Mikrobiologischen Institut, Universitätsklinikum Erlangen, Wasserturmstr. 3-5, 91054 Erlangen, Germany.

出版信息

New Phytol. 2012 Jun;194(4):1046-1060. doi: 10.1111/j.1469-8137.2012.04124.x. Epub 2012 Apr 4.

Abstract

Type III effector proteins (T3Es) of many Gram-negative pathogenic bacteria manipulate highly conserved cellular processes, indicating conservation in virulence mechanisms during the infection of hosts of divergent evolutionary origin. In order to identify conserved effector functions, we used a cross-kingdom approach in which we expressed selected T3Es from the mammalian pathogen Salmonella enterica in leaves of Nicotiana benthamiana and searched for possible virulence or avirulence phenotypes. We show that the T3E SseF of S. enterica triggers hypersensitive response (HR)-like symptoms, a hallmark of effector-triggered immunity in plants, either when transiently expressed in leaves of N. benthamiana by Agrobacterium tumefaciens infiltration or when delivered by Xanthomonas campestris pv vesicatoria (Xcv) through the type III secretion system. The ability of SseF to elicit HR-like symptoms was lost upon silencing of suppressor of G2 allele of skp1 (SGT1), indicating that the S. enterica T3E is probably recognized by an R protein in N. benthamiana. Xcv translocating an AvrRpt2-SseF fusion protein was restricted in multiplication within leaves of N. benthamiana. Bacterial growth was not impaired but symptom development was rather accelerated in a compatible interaction with susceptible pepper (Capsicum annuum) plants. We conclude that the S. enterica T3E SseF is probably recognized by the plant immune system in N. benthamiana, resulting in effector-triggered immunity.

摘要

许多革兰氏阴性病原菌的 III 型效应蛋白(T3Es)操纵高度保守的细胞过程,这表明在宿主进化起源不同的感染过程中,毒力机制具有保守性。为了鉴定保守的效应功能,我们采用了一种跨领域的方法,即将来自哺乳动物病原体沙门氏菌的选定 T3E 在本氏烟的叶片中表达,并寻找可能的毒性或无毒表型。我们表明,沙门氏菌的 T3E SseF 触发了过敏反应(HR)样症状,这是植物中效应触发免疫的标志,当通过根癌农杆菌浸润在本氏烟叶片中瞬时表达时,或者当通过黄单胞菌 pv 番茄(Xcv)通过 III 型分泌系统传递时,均会触发 HR 样症状。SseF 诱导 HR 样症状的能力在沉默 G2 等位基因 skp1(SGT1)的抑制子后丧失,这表明沙门氏菌的 T3E 可能被本氏烟中的 R 蛋白识别。Xcv 易位 AvrRpt2-SseF 融合蛋白在本氏烟叶片内的增殖受到限制。在与易感辣椒(Capsicum annuum)植株的相容互作中,细菌生长不受损害,但症状发展反而加速。我们得出结论,沙门氏菌的 T3E SseF 可能被本氏烟中的植物免疫系统识别,从而引发效应触发免疫。

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