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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.
Theoretical and Applied Genetics ( IF 5.4 ) Pub Date : 2020-01-29 , DOI: 10.1007/s00122-019-03507-w
Min Lin 1 , Beatrice Corsi 2 , Andrea Ficke 3 , Kar-Chun Tan 4 , James Cockram 2 , Morten Lillemo 1
Affiliation  

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.

中文翻译:

使用小麦多创始人群体的遗传作图揭示了染色体 2A 上的一个基因座,该基因座控制对由坏死性真菌病原体 Parastagonospora nodorum 引起的叶片和颖片斑的抗性。

发现小麦染色体 2A 上的一个基因座可以控制对由坏死性真菌病原体 Parastagonospora nodorum 引起的叶片和颖片斑的田间抗性。坏死性真菌病原菌Parastagonospora nodorum 是潮湿和温带地区常见的小麦(Triticum aestivum L.) 病害Septoria nodorum 叶斑病和颖枯病的病原体。对 Septoria nodorum 叶斑病的易感性可以部分解释为对相应的 P. nodorum necrotrophic effectors (NEs) 的敏感性。对颖片的易感性也是定量的;然而,尚未详细研究潜在的遗传学。在这里,我们使用八位创始小麦多亲本高代杂交群体将抗性/易感性基因座遗传映射到叶片和颖片斑。在两个地点和 4 年的六次现场试验中对人群进行了评估。为了比较在受控条件下鉴定的数量性状基因座 (QTL) 与田间鉴定的数量性状基因座 (QTL),还进行了使用三种 P. nodorum 分离株的幼苗浸润和接种试验。在2A和6A染色体上鉴定出3个显着的田间抗性QTL,在2D、5B和7D染色体上鉴定出4个显着的苗期抗性QTL。其中,在挪威和英国检测到QSnb.niab-2A.3 对叶斑病和颖枯病的田间抗性。与来自挪威 P. nodorum 分离株的培养滤液的幼苗反应的 QTL 共置表明 QTL 可能是由新的 NE 敏感性引起的。通过单倍型分析证实了该QTL在幼苗和成株阶段的叶斑病和培养滤液浸润的一致性。然而,叶斑和颖片反应的相反效应表明可能涉及不同的遗传机制。
更新日期:2020-02-14
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