Meta-QTL analysis of tan spot resistance in wheat.

KEY MESSAGE: A total of 19 meta-QTL conferring resistance to tan spot were identified from 104 initial QTL detected in 15 previous QTL mapping studies. Tan spot, caused by the fungal pathogen Pyrenophora tritici-repentis (Ptr), is a major foliar disease worldwide in both bread wheat and durum wheat and can reduce grain yield due to reduction in photosynthetic area of leaves. Developing and growing resistant cultivars is a cost-effective and environmentally friendly approach to mitigate negative effects of the disease. Understanding the genetic basis of tan spot resistance can enhance the development of resistant cultivars. With that goal, over 100 QTL associated with resistance to tan spot induced by a variety of Ptr races and isolates have been identified from previous QTL mapping studies. Meta-QTL analysis can identify redundant QTL among various studies and reveal major QTL for targeting in marker-assisted selection applications. In this study, we performed a meta-QTL analysis of tan spot resistance using the reported QTL from 15 previous QTL mapping studies. An integrated linkage map with a total length of 4080.5 cM containing 47,309 markers was assembled from 21 individual linkage maps and three previously published consensus maps. Nineteen meta-QTL were clustered from 104 initial QTL projected on the integrated map. Three of the 19 meta-QTL located on chromosomes 2A, 3B, and 5A show large genetic effects and confer resistance to multiple races in multiple bread wheat and durum wheat mapping populations. The integration of those race-nonspecific QTL is a promising strategy to provide high and stable resistance to tan spot in wheat.

Genome-wide association mapping of tan spot resistance in a worldwide collection of durum wheat.

KEY MESSAGE: 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.