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效应基因与×种质MAL0004的抗性位点之间可能存在基因对基因的关系。

A putative gene-for-gene relationship between the effector gene and the resistance locus of × accession MAL0004.

作者信息

Emeriewen Ofere Francis, Zetzsche Holger, Wöhner Thomas Wolfgang, Flachowsky Henryk, Peil Andreas

机构信息

Julius Kühn-Institut (JKI), Federal Research Centre for Cultivated Plants, Institute for Breeding Research on Fruit Crops, Dresden, Germany.

Julius Kühn-Institut (JKI), Federal Research Centre for Cultivated Plants, Institute for Resistance Research and Stress Tolerance, Quedlinburg, Germany.

出版信息

Front Plant Sci. 2024 Dec 4;15:1472536. doi: 10.3389/fpls.2024.1472536. eCollection 2024.

Abstract

The bacterial pathogen causes fire blight on rosaceous plants, including apples and their wild relatives. The pathogen uses the type III secretion pathogenicity island to inject effector proteins, such as Eop1, into host plants, leading to disease phenotypes in susceptible genotypes. In contrast, resistant genotypes exhibit quantitative resistance associated with genomic regions and/or R-gene-mediated qualitative resistance to withstand the pathogen. In , strong resistance is observed in some wild species accessions, for example, in accession MAL0004. The resistance locus , previously identified on linkage group 12 (LG12) of MAL0004, is one of two gene loci in proven to withstand highly virulent North American strains of . . This suggests the influence of a major gene, with a few candidate genes proposed within the region. In this report, we provide evidence that this gene locus is completely broken down by a mutant strain of the effector protein Eop1 (Δ) following artificial shoot inoculations of an 'Idared' × MAL0004 F progeny set, indicating a gene-for-gene interaction. Interestingly, Δ does not overcome the resistance of the donor MAL0004 itself, but only the QTL on LG12, an indication that other resistance factors, possibly QTLs/genes are contributing to the fire blight resistance of MAL0004.

摘要

这种细菌病原体可导致包括苹果及其野生近缘种在内的蔷薇科植物发生火疫病。该病原体利用III型分泌致病性岛将效应蛋白(如Eop1)注入宿主植物,从而在易感基因型中导致病害表型。相比之下,抗性基因型表现出与基因组区域相关的数量抗性和/或由R基因介导的质量抗性以抵御病原体。在[具体情况未提及]中,在一些野生种材料中观察到了强抗性,例如在材料MAL0004中。先前在MAL0004的第12连锁群(LG12)上鉴定出的抗性位点,是[具体物种未提及]中已被证明能抵御北美高毒力[具体病原体未提及]菌株的两个基因位点之一。这表明存在一个主基因的影响,并且在[具体区域未提及]区域内提出了一些候选基因。在本报告中,我们提供了证据,在对‘Idared’×MAL0004 F代群体进行人工嫩梢接种后,该基因位点被效应蛋白Eop1的突变菌株(Δ)完全打破,这表明存在基因对基因的相互作用。有趣的是,Δ并不能克服[具体物种未提及]供体MAL0004本身的抗性,而只能克服LG12上的QTL,这表明其他抗性因子,可能是QTL/基因,对MAL0004的火疫病抗性有贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbc3/11656051/201072e8484e/fpls-15-1472536-g001.jpg

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