Inoculation of Malus genotypes with a set of Erwinia amylovora strains indicates a gene‐for‐gene relationship between the effector gene eop1 and both Malus floribunda 821 and Malus ‘Evereste’

Inoculation of Malus genotypes with a set of Erwinia amylovora strains indicates a gene‐for‐gene relationship between the effector gene eop1 and both Malus floribunda 821 and Malus ‘Evereste’
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用一组火梨欧文氏菌菌株接种苹果基因型表明效应基因 eop1 与苹果 floribunda 821 和苹果“Evereste”之间存在基因-基因关系

DOI:
10.1111/ppa.12784
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发表时间:
2018
期刊:
影响因子:
2.7
通讯作者:
Peil A
Peil A
中科院分区:
农林科学2区
文献类型:
--
作者:
Wöhner TW;Richter K;Sundin GW;Zhao Y;Stockwell VO;Sellmann J;Flachowsky H;Hanke M-V;Peil A

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革兰氏阴性细菌梨火疫病菌(Erwinia amylovora)是梨果类果树火疫病的病原菌,它编码一种第三型分泌系统(T3SS),该系统将效应蛋白易位到植物细胞中,这些效应蛋白共同发挥作用以抑制宿主防御并使发病成为可能。到目前为止,只有有限的知识,在几个野生苹果属物种的效应蛋白和宿主抗性的相互作用。本研究用一组效应子缺失突变体菌株和几种高度致病的梨黄孢菌菌株测试了几种苹果属野生种的疾病反应,这些菌株被认为会影响抗火疫病苹果属物种的宿主抗性反应。这些发现证实了早期的研究,即T3SS的缺失消除了病原体的毒力。此外,Eop 1与抗火疫病观赏苹果品种Evereste和野生种海棠a821之间建立了新的基因对基因关系。本研究结果为苹果属植物与病原菌的相互作用提供了新的认识。和食淀粉肠球菌(E. amylovora)。
The Gram‐negative bacteriumErwinia amylovora, causal agent of fire blight disease in pome fruit trees, encodes a type three secretion system (T3SS) that translocates effector proteins into plant cells that collectively function to suppress host defences and enable pathogenesis. Until now, there has only been limited knowledge about the interaction of effector proteins and host resistance presented in several wildMalusspecies. This study tested disease responses in severalMaluswild species with a set of effector deletion mutant strains and several highly virulentE. amylovorastrains, which are assumed to influence the host resistance response of fire blight‐resistantMalusspecies. The findings confirm earlier studies that deletion of the T3SS abolished virulence of the pathogen. Furthermore, a new gene‐for‐gene relationship was established between the effector protein Eop1 and the fire blight resistant ornamental apple cultivar Evereste and the wild speciesMalus floribunda821. The results presented here provide new insights into the host–pathogen interactions betweenMalussp. andE. amylovora.
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