Department of Plant Pathology, North Dakota State University, Fargo, ND, 58108, USA.
Department of Plant Sciences, North Dakota State University, Fargo, ND, 58108, USA.
Theor Appl Genet. 2020 Jul;133(7):2227-2237. doi: 10.1007/s00122-020-03593-1. Epub 2020 Apr 16.
Resistance to tan spot in durum wheat involves race-nonspecific QTL and necrotrophic insensitivity gene. Tan spot, caused by the necrotrophic fungus Pyrenophoratritici-repentis, is a major foliar disease on all cultivated wheat crops worldwide. Compared to common wheat, much less work has been done to investigate the genetic basis of tan spot resistance in durum. Here, we conducted disease evaluations, necrotrophic effector (NE) sensitivity assays and a genome-wide association study using a collection of durum accessions. The durum panel segregated for the reaction to disease inoculations and NE infiltrations with eighteen accessions being highly resistant to all races and most of them insensitive to both PtrToxA and PtrToxB. Over 65,000SNP markers were developed from genotyping-by-sequencing for the association mapping. As expected, sensitivity to PtrToxA and PtrToxB was mapped to the chromosome arms 5BL and 2BS, respectively. For the fungal inoculations, a quantitative trait locus (QTL) on chromosome 3B was associated with resistance to all races and likely corresponds to the race-nonspecific resistance QTL previously identified in common wheat. The Tsn1locus was not significantly associated with tan spot caused by the PtrToxA-producing isolates Pti2 and 86-124, but the Tsc2 locus was significantly associated with tan spot caused by the PtrToxB-producing isolate DW5. Another QTL on chromosome arm 1AS was associated with tan spot caused by the PtrToxC-producing isolate Pti2 and likely corresponds to the Tsc1 locus. Additional QTL for specific races was identified on chromosome 1B and 3B. Our work highlights the complexity of genetic resistance to tan spot and further confirms that the Ptr ToxA-Tsn1 interaction plays no significant role in disease development in tetraploid wheat.
抗赤霉病涉及非专化性 QTL 和坏死型不敏感基因。赤霉病是由半知菌小麦赤霉菌引起的，是全球所有栽培小麦作物的主要叶部病害。与普通小麦相比，对硬粒小麦赤霉病抗性的遗传基础研究要少得多。在这里，我们利用硬粒小麦资源进行了病害评价、坏死型效应物（NE）敏感性测定和全基因组关联研究。硬粒小麦群体对接种的反应和 NE 浸润存在分离，其中 18 个品系对所有小种均高度抗性，其中大多数对 PtrToxA 和 PtrToxB 均不敏感。利用测序分型共开发了超过 65000 个 SNP 标记用于关联作图。如预期的那样，对 PtrToxA 和 PtrToxB 的敏感性分别被定位到 5BL 和 2BS 染色体臂上。对于真菌接种，3B 染色体上的一个数量性状位点（QTL）与对所有小种的抗性有关，可能与之前在普通小麦中鉴定的非专化性抗性 QTL 相对应。Tsn1 位点与由 PtrToxA 产生的分离株 Pti2 和 86-124 引起的赤霉病没有显著关联，但 Tsc2 位点与由 PtrToxB 产生的分离株 DW5 引起的赤霉病显著关联。1AS 染色体臂上的另一个 QTL 与由 PtrToxC 产生的分离株 Pti2 引起的赤霉病有关，可能与 Tsc1 位点相对应。在 1B 和 3B 染色体上还鉴定到了针对特定小种的其他 QTL。我们的工作突出了遗传抗性的复杂性，进一步证实了 Ptr ToxA-Tsn1 相互作用在四倍体小麦中对赤霉病发病没有显著作用。
