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Molecular mapping of resistance to<Emphasis Type="Italic"> Fusarium</Emphasis> head blight in the spring wheat cultivar Frontana
Authors:B?Steiner  M?Lemmens  M?Griesser  U?Scholz  J?Schondelmaier  Email author" target="_blank">H?BuerstmayrEmail author
Institution:(1) Department of Biotechnology in Plant Production, IFA-Tulln, Institute for Agrobiotechnology, Konrad Lorenz Strasse 20, 3430 Tulln, Austria;(2) Saaten-Union Resistenzlabor GmbH, Hovedisser Strasse 92, 33818 Leopoldshoehe, Germany
Abstract: Fusarium head blight (FHB) is a destructive disease of wheat. The objective of this study was to characterise the FHB resistance of the Brazilian spring wheat cultivar Frontana through molecular mapping. A population of 210 doubled-haploid lines from a cross of Frontana (partially resistant) and Remus (susceptible) was evaluated for FHB resistance during three seasons. Spray and single-spikelet inoculations were applied. The severity, incidence and spread of the disease were assessed by visual scoring. The population was genotyped with 566 DNA markers. The major QTL effect associated with FHB resistance mapped to chromosome 3A near the centromere, explaining 16% of the phenotypic variation for disease severity over 3 years. The most likely position is in the Xgwm720–Xdupw227 interval. The genomic region on 3A was significantly associated with FHB severity and incidence in all years evaluated, but not with FHB spread, indicating the prominent contribution of this QTL to resistance against initial infection. The map interval Xgwm129–Xbarc197 on chromosome 5A also showed consistent association with FHB severity and accounted for 9% of the phenotypic variation. In addition, smaller effects for FHB severity were identified on chromosomes 1B, 2A, 2B, 4B, 5A and 6B in single years. Individual QTLs for resistance to FHB spread accounted for less than 10% of the variation in trait expression. The present study indicates that FHB resistance of Frontana primarily inhibits fungal penetration (type I resistance), but has a minor effect on fungal spread after infection (type II resistance).Communicated by H.C. Becker
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