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利用小麦多祖群体进行遗传图谱定位,揭示了控制 2A 染色体上叶枯病和颖枯病的抗坏死真菌病原体禾谷多腔菌的位点。

Genetic mapping using a wheat multi-founder population reveals a locus on chromosome 2A controlling resistance to both leaf and glume blotch caused by the necrotrophic fungal pathogen Parastagonospora nodorum.

机构信息

Department of Plant Sciences, Norwegian University of Life Sciences, Post Box 5003, 1432, Ås, Norway.

John Bingham Laboratory, NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.

出版信息

Theor Appl Genet. 2020 Mar;133(3):785-808. doi: 10.1007/s00122-019-03507-w. Epub 2020 Jan 29.

Abstract

A locus on wheat chromosome 2A was found to control field resistance to both leaf and glume blotch caused by the necrotrophic fungal pathogen Parastagonospora nodorum. The necrotrophic fungal pathogen Parastagonospora nodorum is the causal agent of Septoria nodorum leaf blotch and glume blotch, which are common wheat (Triticum aestivum L.) diseases in humid and temperate areas. Susceptibility to Septoria nodorum leaf blotch can partly be explained by sensitivity to corresponding P. nodorum necrotrophic effectors (NEs). Susceptibility to glume blotch is also quantitative; however, the underlying genetics have not been studied in detail. Here, we genetically map resistance/susceptibility loci to leaf and glume blotch using an eight-founder wheat multiparent advanced generation intercross population. The population was assessed in six field trials across two sites and 4 years. Seedling infiltration and inoculation assays using three P. nodorum isolates were also carried out, in order to compare quantitative trait loci (QTL) identified under controlled conditions with those identified in the field. Three significant field resistance QTL were identified on chromosomes 2A and 6A, while four significant seedling resistance QTL were detected on chromosomes 2D, 5B and 7D. Among these, QSnb.niab-2A.3 for field resistance to both leaf blotch and glume blotch was detected in Norway and the UK. Colocation with a QTL for seedling reactions against culture filtrate from a Norwegian P. nodorum isolate indicated the QTL could be caused by a novel NE sensitivity. The consistency of this QTL for leaf blotch at the seedling and adult plant stages and culture filtrate infiltration was confirmed by haplotype analysis. However, opposite effects for the leaf blotch and glume blotch reactions suggest that different genetic mechanisms may be involved.

摘要

在小麦 2A 染色体上发现了一个控制对叶枯病和颖枯病的田间抗性的基因座,这两种病害均由坏死型真菌病原体禾谷多腔菌引起。坏死型真菌病原体禾谷多腔菌是叶枯病和颖枯病的病原体,这两种病害是潮湿和温带地区普通小麦(Triticum aestivum L.)的常见病。对叶枯病的敏感性部分可以用对相应的禾谷多腔菌坏死型效应物(NEs)的敏感性来解释。对颖枯病的敏感性也是定量的;然而,其潜在的遗传学尚未得到详细研究。在这里,我们使用一个由 8 个亲本组成的小麦多亲本高级世代互交群体,对叶枯病和颖枯病的抗性/敏感性基因座进行遗传作图。该群体在两个地点和 4 年的 6 个田间试验中进行了评估。还进行了使用 3 个禾谷多腔菌分离株的幼苗渗透和接种试验,以便将在受控条件下鉴定的数量性状基因座(QTL)与田间鉴定的 QTL 进行比较。在 2A 和 6A 染色体上鉴定到三个显著的田间抗性 QTL,而在 2D、5B 和 7D 染色体上检测到四个显著的幼苗抗性 QTL。其中,在挪威和英国检测到了对叶枯病和颖枯病都有抗性的 QSnb.niab-2A.3。与对来自挪威禾谷多腔菌分离株的培养滤液的幼苗反应的 QTL 共定位表明,该 QTL 可能是由一种新型的 NE 敏感性引起的。通过单倍型分析证实了该 QTL 在幼苗和成年植株阶段以及培养滤液渗透中的叶枯病一致性。然而,叶枯病和颖枯病反应的相反效果表明,可能涉及不同的遗传机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7021668/033d49cd7517/122_2019_3507_Fig1_HTML.jpg

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