Bread wheat and durum wheat were examined for linkage disequilibrium (LD) using microsatellite markers distributed across the genome. The allele database consisted of 189 bread wheat accessions genotyped at 370 loci and 93 durum wheat accessions genotyped at 245 loci. A significance level of p< 0.001 was set for all comparisons. The bread and durum wheat collections showed that 47.9% and 14.0% of all locus pairs were in LD, respectively. LD was more prevalent between loci on the same chromosome compared with loci on independent chromosomes and was highest between adjacent loci. Only a small fraction (bread wheat, 0.9%; durum wheat, 3.2%) of the locus pairs in LD showed R2 values > 0.2. The LD between adjacent locus pairs extended (R2 > 0.2) approximately 2-3 cM, on average, but some regions of the bread and durum wheat genomes showed high levels of LD (R2 = 0.7 and 1.0, respectively) extending 41.2 and 25.5 cM, respectively. The wheat collections were clustered by similarity into subpopulations using unlinked microsatellite data and the software Structure. Analysis within subpopulations showed 14- to 16-fold fewer locus pairs in LD, higher R2 values for those pairs in LD, and LD extending further along the chromosome. The data suggest that LD mapping of wheat can be performed with simple sequence repeats to a resolution of <5 cM.
Triticum turgidum L var. durum is known to be particularly susceptible to infection by Fusarium graminearum, the causal agent for Fusarium head blight (FHB), which results in severe yield losses and grain contaminated with mycotoxins. This research was aimed at identifying FHB resistance in tetraploid wheat and mapping the location of FHB resistance genes. A tetraploid cross of durum wheat ('Strongfield') x Triticum carthlicum ('Blackbird') was used to generate a doubled-haploid (DH) population. This population was evaluated for type II resistance to F. graminearum in replicated greenhouse trials, in which heads were innoculated and the percent of infected spikelets was determined 21 days later. The population was also genotyped with microsatellite markers to construct a map of 424 loci, covering 2 052 cM. The FHB reaction and genotypic data were used to identify FHB resistance quantitative trait loci (QTLs). It was determined that 2 intervals on chromosomes 2BL and 6BS controlled FHB resistance in this tetraploid cross. The FHB resistance allele on chromosome 2BL (r2=0.26, logarithm of odds (LOD)=8.5) was derived from 'Strongfield', and the FHB resistance allele on chromosome 6BS (r2=0.23, LOD=6.6) was derived from 'Blackbird'. Two other loci, on chromosomes 5AS and 2AL, were shown to regulate FHB infection and to have an epistatic effect on the FHB resistance QTL on chromosome 6BS. Further, the FHB resistance QTL peak on chromosome 6BS was clearly coincident with the known FHB resistance gene Fhb2, derived from Sumai 3. The results show that FHB resistance can be expressed in durum wheat, and that T. carthlicum and Triticum aestivum likely share a common FHB resistance gene on chromosome 6BS.
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