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Stagonospora nodorum is the causal agent of the Stagonospora glume blotch disease in hexaploid wheat. The Swiss winter bread wheat cv. 'Arina' has a highly effective, durable and quantitative glume blotch resistance. We studied 240 single seed descent (SSD)-derived lines of an 'Arina x Forno' F(5:7) population to identify and map quantitative trait loci (QTLs) for glume blotch resistance under natural infestation. Using composite interval mapping (CIM) and LOD>4.5, we detected two chromosomal regions on chromosome arms 3BS and 4BL which were specifically associated with glume blotch resistance. These identified QTLs were designated QSng.sfr-3BS and QSng.sfr-4BL, respectively. QSng.sfr-3BS peaked at the locus Xgwm389 in the telomeric region of the short arm of chromosome 3B and explained 31.2% of the observed phenotypic variance for the resistance within the population. The responsible QSng.sfr-3BS allele originated from the resistant parent 'Arina'. The QTL QSng.sfr-4BL (19.1%) mapped to chromosome arm 4BL ('Forno' allele) very close to two known genes, TaMlo and a catalase ( Cat). Both QTL alleles combined could enhance the resistance level by about 50%. Additionally, they showed significant epistatic effects (4.4%). We found PCR-based microsatellite markers closely linked to QSng.sfr-3BS (gwm389) and QSng.sfr-4BL (gwm251) which make marker-assisted selection (MAS) for Stagonospora glume blotch resistance feasible. We also found one resistance QTL, QSng.sfr-5BL, on the long arm of chromosome 5B which overlapped with QTLs for plant height as well as heading time.
Stagonospora nodorum is the causal agent of the Stagonospora glume blotch disease in hexaploid wheat. The Swiss winter bread wheat cv. 'Arina' has a highly effective, durable and quantitative glume blotch resistance. We studied 240 single seed descent (SSD)-derived lines of an 'Arina x Forno' F(5:7) population to identify and map quantitative trait loci (QTLs) for glume blotch resistance under natural infestation. Using composite interval mapping (CIM) and LOD>4.5, we detected two chromosomal regions on chromosome arms 3BS and 4BL which were specifically associated with glume blotch resistance. These identified QTLs were designated QSng.sfr-3BS and QSng.sfr-4BL, respectively. QSng.sfr-3BS peaked at the locus Xgwm389 in the telomeric region of the short arm of chromosome 3B and explained 31.2% of the observed phenotypic variance for the resistance within the population. The responsible QSng.sfr-3BS allele originated from the resistant parent 'Arina'. The QTL QSng.sfr-4BL (19.1%) mapped to chromosome arm 4BL ('Forno' allele) very close to two known genes, TaMlo and a catalase ( Cat). Both QTL alleles combined could enhance the resistance level by about 50%. Additionally, they showed significant epistatic effects (4.4%). We found PCR-based microsatellite markers closely linked to QSng.sfr-3BS (gwm389) and QSng.sfr-4BL (gwm251) which make marker-assisted selection (MAS) for Stagonospora glume blotch resistance feasible. We also found one resistance QTL, QSng.sfr-5BL, on the long arm of chromosome 5B which overlapped with QTLs for plant height as well as heading time.
Tan spot and Stagonospora nodorum blotch caused by Pyrenophora tritici-repentis (Died.) Drechs. and Phaeosphaeria nodorum (E. M眉 ller) Hedjarroude, respectively, are the major components of the leaf spotting disease complex of durum wheat (Triticum turgidum L.). These diseases induce significant quality and yield reductions and control through host plant resistance is the most effective and economical method. The objectives of this study were to determine the chromosomal locations of major genes conferring resistance to P. tritici-repentis races 1-3 and 5, toxins Ptr ToxA and Ptr ToxB, and P. nodorum isolate Sn2000 in a set of Langdon-Triticum dicoccoides (Israel A) durum substitution lines. Plants were evaluated for disease reaction at the two-leaf stage under controlled environmental conditions. Based on the reactions of the substitution lines, the chromosomal locations of the resistance genes for P. tritici-repentis races 1 and 2, and 3 and 5, were determined to be chromosomes 5B and 3B, respectively. Resistance to toxin Ptr ToxA was located on chromosome 5B whereas toxin Ptr ToxB failed to induce symptoms in the tetraploid genotypes, including the substitution lines. Resistance to P. nodorum isolate Sn2000 was located on chromosome 5B. This is the first study to reveal the chromosomal locations of major genes for resistance to tan spot and Stagonospora nodorum blotch in tetraploid wheat using the Langdon-T. dicoccoides (Israel A) substitution lines.
Stagonospora nodorum blotch (SNB) is an important foliar disease of durum wheat (Triticum turgidum var. durum) worldwide. The combined eVects of SNB and tan spot, considered as components of the leaf spotting disease complex, result in signiWcant damage to wheat production in the northern Great Plains of North America. The main objective of this study was the genetic analysis of resistance to SNB caused by Phaeosphaeria nodorum in tetraploid wheat, and its association with tan spot caused by Pyrenophora tritici-repentis race 2. The 133 recombinant inbred chromosome lines (RICL) developed from the cross LDN/LDN(Dic-5B) were evaluated for SNB reaction at the seedling stage under greenhouse conditions. Molecular markers were used to map a quantitative trait locus (QTL) on chromosome 5B, explaining 37.6% of the phenotypic variation in SNB reaction. The location of the QTL was 8.8 cM distal to the tsn1 locus coding for resistance to P. tritici-repentis race 2. The presence of genes for resistance to both SNB and tan spot in close proximity in tetraploid wheat and the identiWcation of molecular markers linked to these genes or QTLs will be useful for incorporating resistance to these diseases in wheat breeding programs.
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