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Genome-wide association mapping of resistance to the foliar diseases septoria nodorum blotch and tan spot in a global winter wheat collection
Molecular Breeding ( IF 2.6 ) Pub Date : 2023-06-17 , DOI: 10.1007/s11032-023-01400-5
Amanda R Peters Haugrud 1 , Gongjun Shi 2 , Sudeshi Seneviratne 3 , Katherine L D Running 3 , Zengcui Zhang 1 , Gurminder Singh 3 , Agnes Szabo-Hever 1 , Krishna Acharya 3 , Timothy L Friesen 1 , Zhaohui Liu 2 , Justin D Faris 1
Affiliation  

Septoria nodorum blotch (SNB) and tan spot, caused by the necrotrophic fungal pathogens Parastagonospora nodorum and Pyrenophora tritici-repentis, respectively, often occur together as a leaf spotting disease complex on wheat (Triticum aestivum L.). Both pathogens produce necrotrophic effectors (NEs) that contribute to the development of disease. Here, genome-wide association analysis of a diverse panel of 264 winter wheat lines revealed novel loci on chromosomes 5A and 5B associated with sensitivity to the NEs SnTox3 and SnTox5 in addition to the known sensitivity genes for NEs Ptr/SnToxA, SnTox1, SnTox3, and SnTox5. Sensitivity loci for SnTox267 and Ptr ToxB were not detected. Evaluation of the panel with five P. nodorum isolates for SNB development indicated the Snn3-SnTox3 and Tsn1-SnToxA interactions played significant roles in disease development along with additional QTL on chromosomes 2A and 2D, which may correspond to the Snn7-SnTox267 interaction. For tan spot, the Tsc1-Ptr ToxC interaction was associated with disease caused by two isolates, and a novel QTL on chromosome 7D was associated with a third isolate. The Tsn1-ToxA interaction was associated with SNB but not tan spot. Therefore some, but not all, of the previously characterized host gene-NE interactions in these pathosystems play significant roles in disease development in winter wheat. Based on these results, breeders should prioritize the selection of resistance alleles at the Tsc1, Tsn1, Snn3, and Snn7 loci as well as the 2A and 7D QTL to obtain good levels of resistance to SNB and tan spot in winter wheat.



中文翻译:

全球冬小麦收藏中叶部病害斑枯病和棕褐色斑病抗性的全基因组关联图谱

节斑壳针孢 (SNB) 和棕褐色斑病分别由坏死营养型真菌病原体Parastagonospora nodorumPyrenophora tritici-repentis引起,通常作为一种叶斑病复合体一起发生在小麦 ( Triticum aestivum L.) 上。这两种病原体都会产生坏死营养效应子(NE),从而促进疾病的发展。在这里,对 264 个冬小麦品系的不同组进行的全基因组关联分析揭示了除了已知的 NE Ptr/SnToxA、SnTox1、SnTox3、和SnTox5。未检测到 SnTox267 和 Ptr ToxB 的敏感位点。对五个P. nodorum分离株进行 SNB 发育的评估表明,Snn3 -SnTox3 和Tsn1 -SnToxA 相互作用以及 2A 和 2D 染色体上的额外 QTL(可能对应于 Snn7 -SnTox267相互作用)在疾病发展中发挥着重要作用。对于棕褐色斑,Tsc1 -Ptr ToxC 相互作用与两个分离株引起的疾病相关,并且 7D 染色体上的新 QTL 与第三个分离株相关。Tsn1 -ToxA 相互作用与 SNB 相关,但与棕褐色斑无关因此,先前表征的这些病理系统中的一些(但不是全部)宿主基因-NE 相互作用在冬小麦疾病发展中发挥着重要作用。基于这些结果,育种者应优先选择Tsc1Tsn1Snn3Snn7位点以及2A和7D QTL的抗性等位基因,以获得良好水平的冬小麦对SNB和棕斑病的抗性。

更新日期:2023-06-20
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