Abstract

ABSTRACTControl 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.

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