Molecular mapping of novel genes controlling Fusarium head blight resistance and deoxynivalenol accumulation in spring wheat
- PMID: 12897863
- DOI: 10.1139/g03-033
Molecular mapping of novel genes controlling Fusarium head blight resistance and deoxynivalenol accumulation in spring wheat
Abstract
Fusarium head blight of wheat is an extremely damaging disease, causing severe losses in seed yield and quality. The objective of the current study was to examine and characterize alternate sources of resistance to Fusarium head blight (FHB). Ninety-one F1-derived doubled haploid lines from the cross Triticum aestivum 'Wuhan-1' x Triticum aestivum 'Maringa' were examined for disease reaction to Fusarium graminearum by single-floret injection in replicated greenhouse trials and by spray inoculation in replicated field trials. Field and greenhouse experiments were also used to collect agronomic and spike morphology characteristics. Seed samples from field plots were used for deoxynivalenol (DON) determination. A total of 328 polymorphic microsatellite loci were used to construct a genetic linkage map in this population and together these data were used to identify QTL controlling FHB resistance, accumulation of DON, and agronomic and spike morphology traits. The analysis identified QTL for different types of FHB resistance in four intervals on chromosomes 2DL, 3BS, and 4B. The QTLs on 4B and 3BS proximal to the centromere are novel and not reported elsewhere. QTL controlling accumulation of DON independent of FHB resistance were located on chromosomes 2DS and 5AS. Lines carrying FHB resistance alleles on 2DL and 3BS showed a 32% decrease in disease spread after single-floret injection. Lines carrying FHB resistance alleles on 3BS and 4B showed a 27% decrease from the mean in field infection. Finally, lines carrying favourable alleles on 3BS and 5AS, showed a 17% reduction in DON accumulation. The results support a polygenic and quantitative mode of inheritance and report novel FHB resistance loci. The data also suggest that resistance to FHB infection and DON accumulation may be controlled, in part, by independent loci and (or) genes.
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