Abstract
Soil-borne wheat mosaic virus (SBWMV) causes a serious viral disease that can significantly reduce grain yield in winter wheat worldwide. Using resistant cultivars is the only feasible strategy to reduce the losses caused by SBWMV. To fine map the resistance gene Sbwm1, 205 wheat accessions was genotyped using wheat Infinium iSelect Beadchips with 90 K SNPs. Association analysis identified 35 SNPs in 12 wheat genes and one intergenic SNP in the Sbwm1 region that showed a significant association with SBWMV resistance. Those SNPs were converted into Kompetitive Allele-Specific Polymerase assays (KASP) and analyzed in two F6-derived recombinant inbred line (RIL) populations derived from the crosses between two resistant cultivars ‘Wesley’ and ‘Deliver’ and a susceptible line ‘OK03825-5403-6’. Linkage analysis mapped this gene on chromosome 5D at intervals of 5.1 cM and 3.4 cM in the two populations, respectively. The two flanking markers in both populations delimited the gene to a 620 kb region where 19 genes were annotated. Comparative analysis identified a syntenic region of 660 kb in Ae. tauschii with 18 annotated genes and a syntenic region in chromosome 1 of B. distachyon. The candidate region includes several disease resistance related genes and we identified a PTI1-like tyrosine-protein kinase 1 gene as a putative candidate gene for Sbwm1. The two flanking SNPs for Sbwm1 can effectively separate the resistant and susceptible lines in a new diversity panel of 159 wheat germplasm. The results from this study lay a solid foundation for the cloning, functional characterization and marker-assisted selection of Sbwm1.
Highlights
Soil-borne wheat mosaic (SBWM) disease, caused by Soil-borne wheat mosaic virus (SBWMV) was first appeared in the Great Plains of the U.S.A. in 19191 and has become an important disease in most winter wheat growing regions globally[2,3,4,5,6,7]
High correlation coefficients were observed for SBWMV resistance between the two years of phenotypic data from the marker validation population (r = 0.92, p < 0.01), the two recombinant inbred line (RIL) populations (r = 0.81 and 0.94, p < 0.01), and the association mapping population (r = 0.85, p < 0.01)[17], suggesting a high repeatability of SBWMV resistance data between the field experiments
In the two biparental populations, the distribution of SBWMV disease scores deviated significantly from a normal distribution and showed an obvious bimodal distribution with two peaks towards the resistant and susceptible parents (Fig. 1), suggesting that a major gene is responsible for SBWMV resistance in Wesley and Deliver
Summary
Soil-borne wheat mosaic (SBWM) disease, caused by Soil-borne wheat mosaic virus (SBWMV) was first appeared in the Great Plains of the U.S.A. in 19191 and has become an important disease in most winter wheat growing regions globally[2,3,4,5,6,7]. Polymyxa graminis is one of the endoparasitic slime molds (Plasmodiophoromycota), which can produce resting spores that harbor viral RNA and movement protein, and can be distributed by wind, water and machinery Those resting virus-containing spores can remain dormant and invasive in soil for up to 30 years, and germinate in an environment favorable for infection when host are available. With the rapid development and wide use of molecular markers in wheat genetic studies, quantitative trait locus (QTL) mapping approach has been used to localize SBWMV resistance genes using linkage maps. A gene conferring resistance to Soil-borne cereal mosaic virus (SBCMV) in ‘Cadenza’, ‘Tremie’ and ‘Claire’, designated as Sbm[1], was mapped in the region of Sbwm[119,20]. SNP chips with various number of SNPs including Wheat 9 K iSelect, Wheat 90 K iSelect and Wheat 660 K Axiom SNP chips have been developed and widely used to map genes or QTLs for different traits[24,25,26,27,28]
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