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Control of Fusarium head blight (FHB), incited primarily by Fusarium graminearum Schwabe [telomorph Gibberella zea (Schwein)], has been a challenge for barley (Hordeum vulgare L.) producers in the upper midwestern United States for more than a decade. This disease manifests primarily in the form of food safety issues and quality discounts due to the presence of deoxynivalenol (DON), a mycotoxin produced by the pathogen. Cultural practices and fungicides only provide partial control; genetic resistance to FHB and DON accumulation may add to control of the disease. Field studies in North Dakota and China were conducted in FHB disease nurseries using 118 double-haploid lines from the cross C93-3230-24/'Foster'. Foster is susceptible to FHB, and C93-3230-24 is moderately resistant. The quantitative trait locus (QTL) analysis revealed five putative QTL for Type I FHB resistance; however, only the one in bins 7 and 8 of chromosome 2H was detected in more than 70% of the environments. In addition, QTL associated with late days to heading and maturity and tall plant height also were located in the same region. Three putative QTL for increased DON accumulation were detected; however, none were detected in more than three of the eight environments where data were collected. On the basis of these results, it is unlikely that C93-3230-24 has a novel QTL for FHB resistance different from those identified in other resistant accessions. However, C93-3230-24 is unique in that it provides QTL for improved FHB resistance but not reduced DON accumulation. This is an atypical response compared with other sources of FHB resistance and provides evidence that FHB resistance and DON accumulation are under separate genetic control.

Molecular marker technology shows potential to select and combine favorable alleles via genotypic selection and can be used to develop improved crop cultivars with considerable resource savings. In the present investigation, the utility of molecular markers for net blotch resistance identified in Australian breeding material was investigated for Canadian breeding material. Screening 42 Canadian, Australian, and international barley (Hordeum vulgare L.) lines with 10 Canadian Pyrenophora teres Drechs. isolates identified three lines resistant to all isolates evaluated. Net-form net blotch isolates were more virulent than spot-form net blotch isolates. The strong agreement between seedling and adult-plant reactions indicated that seedling screening could be useful for selection for adult-plant resistance. Evaluation of the inheritance of resistance in four Australian populations against Canadian P. teres isolates revealed one to three resistance genes, depending on the isolate used. The majority of Australian barley mapping population parents were susceptible to Canadian P. teres isolates, suggesting markers linked to their resistance may not be useful for Canadian breeding; however, some molecular markers identified by Australian workers could be used for Canadian barley breeding. This study demonstrates that the differences in germplasm and fungal pathogen strains used in different countries result in molecular markers that may not be applicable in all breeding programs for that crop.

Inheritance studies on the nonhost resistance of plants would normally require interspecific crosses that suffer from sterility and abnormal segregation. Therefore, we developed the barley-Puccinia rust model system to study, using forward genetics, the specificity, number, and diversity of genes involved in nonhost resistance. We developed two mapping populations by crossing the line SusPtrit, with exceptional susceptibility to heterologous rust species, with the immune barley cultivars Vada and Cebada Capa. These two mapping populations along with the Oregon Wolfe Barley population, which showed unexpected segregation for resistance to heterologous rusts, were phenotyped with four heterologous rust fungal species. Positions of QTL conferring nonhost resistance in the three mapping populations were compared using an integrated consensus map. The results confirmed that nonhost resistance in barley to heterologous rust species is controlled by QTL with different and overlapping specificities and by an occasional contribution of an R-gene for hypersensitivity. In each population, different sets of loci were implicated in resistance. Few genes were common between the populations, suggesting a high diversity of genes conferring nonhost resistance to heterologous pathogens. These loci were significantly associated with QTL for partial resistance to the pathogen Puccinia hordei and with defense-related genes.