ABSTRACT
An association genetics analysis was conducted to investigate the genetics of resistance to Septoria tritici blotch, caused by the fungus Zymoseptoria tritici (alternatively Mycosphaerella graminicola), in cultivars and breeding lines of wheat (Triticum aestivum) used in the UK between 1860 and 2000. The population was tested with Diversity Array Technology (DArT) and simple-sequence repeat (SSR or microsatellite) markers. The lines formed a single population with no evidence for subdivision, because there were several common ancestors of large parts of the pedigree. Quantitative trait loci (QTLs) controlling Septoria resistance were postulated on 11 chromosomes, but 38% of variation was not explained by the identified QTLs. Calculation of best linear unbiased predictions (BLUPs) identified lineages of spring and winter wheat carrying different alleles for resistance and susceptibility. Abundant variation in Septoria resistance may be exploited by crossing well-adapted cultivars in different lineages to achieve transgressive segregation and thus breed for potentially durable quantitative resistance, whereas phenotypic selection for polygenic quantitative resistance should be effective in breeding cultivars with increased resistance. The most potent allele reducing susceptibility to Septoria, on chromosome arm 6AL, was associated with reduced leaf size. Genes which increase susceptibility to Septoria may have been introduced inadvertently into UK wheat breeding programmes from cultivars used to increase yield, rust resistance and eyespot resistance between the 1950s and 1980s. This indicates the need to consider trade-offs in plant breeding when numerous traits are important and to be cautious about the use of non-adapted germplasm.
Subject(s)
Ascomycota/physiology , Disease Resistance , Plant Diseases/immunology , Plant Diseases/microbiology , Triticum/immunology , Triticum/microbiology , Breeding , Chromosomes, Plant/genetics , Disease Resistance/genetics , Disease Susceptibility , Genetic Markers , Genotype , Inheritance Patterns/genetics , Linkage Disequilibrium/genetics , Microsatellite Repeats/genetics , Models, Genetic , Phenotype , Plant Leaves/anatomy & histology , Quantitative Trait, Heritable , Triticum/anatomy & histology , Triticum/geneticsABSTRACT
Segregation of partial resistance to Pseudomonas syringae pv. maculicola (Psm) ES4326 was studied in the recombinant inbred population created from accessions (ecotypes) Columbia (Col-4), the more susceptible parent, and Landsberg (Ler-0). Plants were spray inoculated with lux-transformed bacteria in experiments to measure susceptibility. The amount of disease produced on a range of Col × Ler lines by spray inoculation was highly correlated with that produced by pressure infiltration of bacteria into the apoplast. Quantitative trait locus (QTL) analysis identified four loci that contributed to partial resistance: QRpsJIC-1.1, QRpsJIC-2.1, QRpsJIC-3.1 and QRpsJIC-5.1 on chromosomes 1, 2, 3 and 5, respectively. QRpsJIC-3.1, located 8.45 cM from the top of the consensus genetic map of chromosome 3, had a large, approximately additive effect on partial resistance, explaining 50% of the genetic variation in this population. Fine mapping narrowed the region within which this QTL was located to 62 genes. A list of candidate genes included several major classes of resistance gene.
