Shankar, M., Walker, E., Golzar, H., Loughman, R., Wilson, R. E., and Francki, M. G. 2008. Quantitative trait loci for seedling and adult plant resistance to Stagonospora nodorum in wheat. Phytopathology 98:886-893.Stagonospora nodorum blotch (SNB) caused by Stagonospora nodorum is a severe disease of wheat (Triticum aestivum) in many areas of the world. S. nodorum affects both seedling and adult plants causing necrosis of leaf and glume tissue, inhibiting photosynthetic capabilities, and reducing grain yield. The aims of this study were to evaluate disease response of 280 doubled haploid (DH) individuals derived from a cross between resistant (6HRWSN125) and susceptible (WAWHT2074) genotypes, compare quantitative trait loci (QTL) for seedling and adult plant resistance in two consecutive years, and assess the contribution of QTL on grain weight. Flag leaves and glumes of individuals from the DH population were inoculated with mixed isolates of S. nodorum at similar maturity time to provide accurate disease evaluation independent of morphological traits and identify true resistance for QTL analysis. Fungicide protected and inoculated plots were used to measure relative grain weight (RGW) as a yield-related trait under pathogen infection. The lack of similar QTL and little or no correlation in disease scores indicate different genes control seedling and adult plant disease and independent genes control flag leaf and glume resistance. This study consistently identified a QTL on chromosome 2DL for flag leaf resistance (QSnl.daw-2D) and 4BL for glume resistance (QSng.daw-4B) from the resistant parent, 6HRWSN125, explaining 4 to 19% of the phenotypic variation at each locus. A total of 5 QTL for RGW were consistently detected, where two were in the same marker interval for QSnl.daw-2D and QSng.daw-4B indicating the contribution of these QTL to yield related traits. Therefore, RGW measurement in QTL analysis could be used as a reliable indicator of grain yield affected by S. nodorum infection.

The slow rate of genetic gain for improving resistance to Septoria nodorum blotch (SNB) is due to the inherent complex interactions between host, isolates, and environments. Breeding for improved SNB resistance requires evaluation and selection of wheat genotypes consistently expressing low SNB response in different target production environments. The study focused on evaluating 232 genotypes from global origins for resistance to SNB in the flag leaf expressed in different Western Australian environments. The aim was to identify resistant donor germplasm against historical and contemporary pathogen isolates and enhance our knowledge of the genetic basis of genotype-byenvironment interactions for SNB response. Australian wheat varieties, inbred lines from Centro Internacional de Mejoramiento de Maiz y Trigo (CIMMYT), and International Center for Agricultural Research in the Dry Areas (ICARDA), and landraces from discrete regions of the world showed low to moderate phenotypic correlation for disease response amongst genotypes when evaluated with historical and contemporary isolates at two locations across 3 years in Western Australia (WA). Significant (P < 0.001) genotype-by-environment interactions were detected regardless of same or different isolates used as an inoculum source. Joint regression analysis identified 19 genotypes that consistently expressed low disease severity under infection with different isolates in multi-locations. The CIMMYT inbred lines, 30ZJN09 and ZJN12 Qno25, were particularly pertinent as they had low SNB response and highest trait stability at two locations across 3 years. Genome wide association studies detected 20 QTL associated with SNB resistance on chromosomes 1A, 1B, 4B, 5A, 5B, 6A, 7A, 7B, and 7D. QTL on chromosomes 1B and 5B were previously reported in similar genomic regions. Multiple QTL were identified on 1B, 5B, 6A, and 5A and detected in response to SNB infection against different isolates and specific environments. Known SnTox-Snn interactions were either not evident or variable across WA environments and SNB response may involve other multiple complex biological mechanisms.

A number of technologies are available to increase the abundance of DNA markers and contribute to developing high resolution genetic maps suitable for genetic analysis. The aim of this study was to expand the number of Diversity Array Technology (DArT) markers on the wheat array that can be mapped in the wheat genome, and to determine their chromosomal location with respect to simple sequence repeat (SSR) markers and their position on the cytogenetic map. A total of 749 and 512 individual DArT and SSR markers, respectively, were identified on at least one of four genetic maps derived from recombinant inbred line (RIL) or doubled haploid (DH) populations. A number of clustered DArT markers were observed in each genetic map, in which 20-34% of markers were redundant. Segregation distortion of DArT and SSR markers was also observed in each mapping population. Only 14% of markers on the Version 2.0 wheat array were assigned to chromosomal bins by deletion mapping using aneuploid lines. In this regard, methylation effects need to be considered when applying DArT marker in genetic mapping. However, deletion mapping of DArT markers provides a reference to align genetic and cytogenetic maps and estimate the coverage of DNA markers across the wheat genome.

Stagonospora nodorum blotch (SNB) is a significant disease in some wheat-growing regions of the world. Resistance in wheat to Stagonospora nodorum is complex, whereby genes for seedling, flag leaf, and glume resistance are independent. The aims of this study were to identify alternative genes for flag leaf resistance, to compare and contrast with known quantitative trait loci (QTL) for SNB resistance, and to determine the potential role of host-specific toxins for SNB QTL. Novel QTL for flag leaf resistance were identified on chromosome 2AS inherited from winter wheat parent ‘P92201D5’ and chromosome 1BS from spring wheat parent ‘EGA Blanco’. The chromosomal map position of markers associated with QTL on 1BS and 2AS indicated that they were unlikely to be associated with known host–toxin insensitivity loci. A QTL on chromosome 5BL inherited from EGA Blanco had highly significant association with markers fcp001 and fcp620 based on disease evaluation in 2007 and, therefore, is likely to be associated with Tsn1-ToxA insensitivity for flag leaf resistance. However, fcp001 and fcp620 were not associated with a QTL detected based on disease evaluation in 2008, indicating two linked QTL for flag leaf resistance with multiple genes residing on 5BL. This study identified novel QTL and their effects in controlling flag leaf SNB resistance.

Resistance to stagonospora nodorum blotch (SNB) in glumes of hexaploid wheat (Triticum aestivum L.), caused by Phaeosphaeria (Stagonospora anamorph) nodorum was investigated in a recombinant‐inbred (RI) population. The Purdue University winter wheat breeding lines P91193D1 and P92201D5, unrelated by parentage but both exhibiting partial SNB resistance, were crossed to develop 254 RI lines by single‐seed descent (SSD) from a random population of F2 plants, to identify quantitative trait loci (QTLs) controlling SNB resistance in wheat glumes. The RI population, together with parent lines, was phenotyped for glume resistance to SNB under field conditions in F8:10 at Evansville, Vincennes, and Lafayette, IN, in 2003; in F7:9 at South Perth, Australia, in 2004; and in F8:10 in greenhouse‐grown inoculated tests at Lafayette in 2003 and 2004. Two QTLs for resistance to SNB in glumes were identified: QSng.pur‐2DL.1 from P91193D1 and QSng.pur‐2DL.2 from P92201D5. The QTL QSng.pur‐2DL.1 explained from 12.3% of the phenotypic variation for resistance in southern Indiana (Evansville and Vincennes) to 38.1% at South Perth; QSng.pur‐2DL.2 accounted for 6.9 and 11.2% of the phenotypic variation in Indiana and South Perth, respectively. This study is the first report of SNB glume blotch resistance in which the same QTLs were identified in tests on different continents where Stagonospora nodorum populations are probably genetically diverse.

The genetic control of adult plant resistance to Stagonospora nodorum blotch (SNB) is complex, consisting of genes with minor effects interacting in an additive manner. Earlier studies detected quantitative trait loci (QTL) for flag leaf resistance in successive years on chromosomes 1B, 2A, 2D, and 5B using SSR- and DArT-based genetic maps of progeny from the crosses EGA Blanco/Millewa, 6HRWSN125/WAWHT2074, and P92201D5/P91193D1. Similarly, QTL for glume resistance detected in successive years and multiple environments were identified on chromosomes 2D and 4B from genetic maps of P92201D5/P91193D1 and 6HRWSN125/WAWHT2074, respectively. The SSR- and DArT-based genetic maps had an average distance of 6.5, 7.8, and 9.7 cM between marker loci for populations EGA/Millewa, P92201D5/P91193D1, and 6HRWSN125/WAWHT2074, respectively. This study used single nucleotide polymorphism (SNP) markers from the iSelect Infinium 90K genotyping array to fine-map genomic regions harbouring QTL for flag leaf and glume SNB resistance, reducing the average distance between markers to 2.9, 3.3, and 3.4 cM for populations P92201D5/P91193D1, EGA/Millewa, and 6HRWSN125/WAWHT2074, respectively. Increasing the marker density of the genetic maps with SNPs did not identify any new QTL for SNB resistance but discriminated previously identified co-located QTL into separate but closely linked QTL.

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Chromosome 1R of rye is a useful source of genes for disease resistance and enhanced agronomic performance in wheat. One of the most prevalent genes transferred to wheat from rye is the stem rust resistance gene Sr31. The recent emergence and spread of a stem rust pathotype virulent to this gene has refocused efforts to find and utilize alternative sources of resistance. There has been considerable effort to transfer a stem rust resistance gene, SrR, from Imperial rye, believed to be allelic to Sr31, into commercial wheat cultivars. However, the simultaneous transfer of genes at the Sec-1 locus encoding secalin seed storage proteins and their association with quality defects preclude the deployment of SrR in some commercial wheat breeding programs. Previous attempts to induce homoeologous recombination between wheat and rye chromosomes to break the linkage between SrR and Sec-1 whilst retaining the tightly linked major loci for wheat seed storage proteins, Gli-D1 and Glu-D3, and recover good dough quality characteristics, have been unsuccessful. We produced novel tertiary wheat-rye recombinant lines carrying different lengths of rye chromosome arm 1RS by inducing homoeologous recombination between the wheat 1D chromosome and a previously described secondary wheat-rye recombinant, DRA-1. Tertiary recombinant T6-1 (SrR+ Sec-1-) carries the target gene for stem rust resistance from rye and retains Gli-D1 but lacks the secalin locus. The tertiary recombinant T49-7 (SrR- Sec-1+) contains the secalin locus but lacks the stem rust resistance gene. T6-1 is expected to contribute to wheat breeding programs in Australia, whereas T49-7 provides opportunities to investigate whether the presence of secalins is responsible for the previously documented dough quality defects.