Peters Haugrud Amanda R, Shi Gongjun, Seneviratne Sudeshi, Running Katherine L D, Zhang Zengcui, Singh Gurminder, Szabo-Hever Agnes, Acharya Krishna, Friesen Timothy L, Liu Zhaohui, Faris Justin D
Cereal Crops Research Unit, Edward T. Schafer Agricultural Research Center, Agricultural Research Service, United States Department of Agriculture, , Fargo, ND 58102 USA.
Department of Plant Pathology, North Dakota State University, Fargo, ND 58102 USA.
Mol Breed. 2023 Jun 17;43(7):54. doi: 10.1007/s11032-023-01400-5. eCollection 2023 Jul.
Septoria nodorum blotch (SNB) and tan spot, caused by the necrotrophic fungal pathogens and , respectively, often occur together as a leaf spotting disease complex on wheat ( 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 isolates for SNB development indicated the -SnTox3 and -SnToxA interactions played significant roles in disease development along with additional QTL on chromosomes 2A and 2D, which may correspond to the -SnTox267 interaction. For tan spot, the -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 -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 , , , and loci as well as the 2A and 7D QTL to obtain good levels of resistance to SNB and tan spot in winter wheat.
The online version contains supplementary material available at 10.1007/s11032-023-01400-5.
小麦颖枯病（SNB）和黄斑病分别由坏死营养型真菌病原体引起，在小麦上常作为叶斑病复合体同时发生。两种病原体都会产生有助于疾病发展的坏死营养型效应子（NEs）。在此，对264个冬小麦品系的多样化群体进行全基因组关联分析，除了已知的NEs Ptr/SnToxA、SnTox1、SnTox3和SnTox5的敏感基因外，还揭示了5A和5B染色体上与对NEs SnTox3和SnTox5敏感性相关的新位点。未检测到SnTox267和Ptr ToxB的敏感位点。用5种分离株对该群体进行小麦颖枯病发展评估表明，-SnTox3和-SnToxA相互作用在疾病发展中起重要作用，同时在2A和2D染色体上还有其他数量性状位点（QTL），这可能与-SnTox267相互作用相对应。对于黄斑病，-Ptr ToxC相互作用与两种分离株引起的疾病相关，7D染色体上的一个新QTL与第三种分离株相关。-ToxA相互作用与小麦颖枯病相关，但与黄斑病无关。因此，这些病理系统中一些（但不是全部）先前鉴定的宿主基因-NE相互作用在冬小麦疾病发展中起重要作用。基于这些结果，育种者应优先选择、、、和位点以及2A和7D QTL上的抗性等位基因，以获得冬小麦对小麦颖枯病和黄斑病的良好抗性水平。
在线版本包含可在10.1007/s11032-023-01400-5获取的补充材料。
