Determining the Order of Resistance Genes Qsng-3BS, Fhb1 and Sr2 and Combining Them in Coupling on Wheat Chromosome 3BS
A variety of diseases of wheat (Triticum aestivum L.) occurs every year in the U.S. leading to significant grain yield losses. Stagonospora nodorum blotch (SNB), fusarium head blight (FHB) and stem rust (SR) are caused by the fungi Stagonospora nodorum, Fusarium graminearum and Puccinia graminis, respectively. These diseases penalize both grain yield and quality. Three resistance factors, Qsng.sfr-3BS, Fhb1 and Sr2 conferring resistance, respectively, to SNB, FHB and SR, each from a unique donor wheat parent line, have been mapped to chromosome 3BS of wheat and are believed to be closely linked. Based on previously published analyses, Sr2 is on the distal end, Fhb1 is on the proximal end and Qsng.sfr-3BS is in the middle of Sr2 and Fhb1 in the 3BS wheat genome. Thus, the objectives of this project are to determine the gene order of Qsng.sfr-3BS, Fhb1 and Sr2, in a linkage block on chromosome 3BS and combining them in coupling. The linkage relationships were determined through analysis of a three-way cross between parental lines Arina, Alsen and Ocoroni86, containing the resistance genes Qsng.sfr-3BS, Fhb1 and Sr2, respectively. A total of 1,600 F2 plants was screened, along with the parental lines, using KASPar genotyping technology via single-nucleotide polymorphism markers to identify the recombinant progeny. Phenotypic screening for SNB was performed on the entire F2 population. Knowing the positional order of these resistance genes will enable the development of a wheat line with three genes in coupling to provide durable and broad-spectrum resistance against three major diseases of wheat.
KeywordsQuantitative Trait Locus Fusarium Head Blight Stem Rust Fusarium Head Blight Resistance Resistance Quantitative Trait Locus
Stagonospora nodorum blotch (SNB), fusarium head blight (FHB) and stem rust (SR) of wheat are caused by the fungi Stagonospora nodorum, Fusarium graminearum and Puccinia graminis, respectively. Each of these diseases can cause yield losses up to 50 % or more during severe epidemics and when environmental conditions are favorable (Chester 1943; Roefls 1978; Stakman and Harrar 1957; Wicki et al. 1999). In addition to yield reduction, FHB reduces quality due to production of a mycotoxin called vomitoxin (deoxynivalenol) produced by F. graminearum (Bai et al. 2001; Gilbert and Tekauz 2000), which is harmful to both humans and livestock. FHB also reduces test weight and lowers market grade. Thus, FHB is one of the most feared fungal diseases of wheat because an entire crop can be rejected for human consumption due to mycotoxin contamination. SR has a capacity of destroying millions of hectares of healthy, high-yielding wheat in less than a month by reducing fields to a mass of bare stalks supporting only small, shriveled grains by harvest time (Singh et al. 2008). There have been several epidemics of SR during the past 80 years that have reduced the yield by 50 % in the Great Plains (Chester 1943; Roefls 1978; Stakman and Harrar 1957). SNB is one of the major foliar and glume diseases of wheat and the most yield loss occurs when the flag leaf and the two leaves below the flag leaf become infected by the time the wheat flowers in late May.
The objective of this study is to find the gene order of Fhb1, Sr2 and Qsng.sfr-3BS with the long-term goal of combining them in a linkage block on wheat chromosome 3BS. The first objective was achieved by crossing three unique parental lines with resistance genes Fhb1, Sr2 and Qsng.sfr-3BS to combine them into one background. An F2 population segregating for all three genes was genotyped with single-nucleotide polymorphism (SNP) markers to validate the presence of markers linked to the resistance genes and also to determine the gene order. The F2 population was also phenotyped for level of resistance to SNB.
Materials and Methods
The mapping population consisted of 1,600 F2 progeny derived from a three-way cross between wheat cultivars Arina, Alsen and Ocoroni86 providing the resistance genes Qsng.sfr-3BS, Fhb1, and Sr2, respectively. The F2 population, its parents and cultivar Chinese Spring as negative control, were planted in January, 2013 in a greenhouse at Purdue University in West Lafayette, Indiana, U.S.A.. The primary spike after spike emergence (Feekes growth stage 10.3) of an adult plant of every F2 progeny and the parental lines was phenotyped in a greenhouse using an isolate of S. nodorum obtained from an infected wheat field in Indiana. The disease severity scores were recorded 21 days after inoculation on a 0–9 scale. The F2 plants were screened along with the parental lines using KASPar genotyping technology to identify the recombinant plants. Single-nucleotide polymorphism markers were utilized to identify the recombinants, determine the gene order, to make the genetic map and for quantitative trait loci (QTL) analysis. Linkage analysis was performed and the map was made with JoinMap 3.0.
Results and Discussion
Phenotyping of all 1,600 F2 progeny was performed and the results utilized the full range of the 0–9 disease-rating scale. The frequency distribution of the percent diseased glume tissue of F2 progeny derived from the three-way cross of Arina (containing the Qsng.sfr-3BS SNB resistance QTL), Alsen and Ocoroni86 inoculated with a field isolate of S. nodorum in a greenhouse showed a continuous distribution with a skew towards susceptibility, indicating the presence of one or more QTL for resistance (data not shown).
- Chester KS (1943) The decisive influence of late winter wheat on wheat leaf rust epiphytotics. Plant Dis Rep Suppl 143:133–44Google Scholar
- Roefls AP (1978) Estimated losses caused by rust in small grain cereals in the United States-1918-76, vol 1363, Miscellaneous publication (United States. Department of Agriculture). U.S. Department of Agriculture, Agricultural Research Service, Washington, DC, 85 ppGoogle Scholar
- Stakman EC, Harrar JC (1957) Principles of plant pathology. Ronald Press, New York, 553 ppGoogle Scholar
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