SummaryWhite mould of soya bean, caused by Sclerotinia sclerotiorum (Lib.) de Bary, is a necrotrophic fungus capable of infecting a wide range of plants. To dissect the genetic architecture of resistance to white mould, a high‐density customized single nucleotide polymorphism (SNP) array (52 041 SNPs) was used to genotype two soya bean diversity panels. Combined with resistance variation data observed in the field and greenhouse environments, genome‐wide association studies (GWASs) were conducted to identify quantitative trait loci (QTL) controlling resistance against white mould. Results showed that 16 and 11 loci were found significantly associated with resistance in field and greenhouse, respectively. Of these, eight loci localized to previously mapped QTL intervals and one locus had significant associations with resistance across both environments. The expression level changes in genes located in GWAS‐identified loci were assessed between partially resistant and susceptible genotypes through a RNA‐seq analysis of the stem tissue collected at various time points after inoculation. A set of genes with diverse biological functionalities were identified as strong candidates underlying white mould resistance. Moreover, we found that genomic prediction models outperformed predictions based on significant SNPs. Prediction accuracies ranged from 0.48 to 0.64 for disease index measured in field experiments. The integrative methods, including GWAS, RNA‐seq and genomic selection (GS), applied in this study facilitated the identification of causal variants, enhanced our understanding of mechanisms of white mould resistance and provided valuable information regarding breeding for disease resistance through genomic selection in soya bean.
Pythium root rot is one of the significant diseases of soybean (Glycine max (L.) Merr.) in the United States. The causal agent of the disease is a soil-borne oomycete pathogen Pythium irregulare, the most prevalent and aggressive species of Pythium in North Central United States. However, few studies have been conducted in soybean for the identification of quantitative trait loci (QTL) for tolerance to P. irregulare. In this study, two recombinant inbred line (RIL) populations (designated as POP1 and POP2) were challenged with P. irregulare (isolate CMISO2-5-14) in a greenhouse assay. POP1 and POP2 were derived from ‘E09014’ × ‘E05226-T’ and ‘E05226-T’ × ‘E09088’, and contained 113 and 79 lines, respectively. Parental tests indicated that ‘E05226-T’ and ‘E09014’ were more tolerant than ‘E09088’, while ‘E09088’ was highly susceptible to the pathogen. The disease indices, root weight of inoculation (RWI) and ratio of root weight (RRW) of both populations showed near normal distributions, with transgressive segregation, suggesting the involvement of multiple QTL from both parents contributed to the tolerance. All the lines were genotyped using Illumina Infinium BARCSoySNP6K iSelect BeadChip and yielded 1373 and 1384 polymorphic markers for POP1 and POP2, respectively. Notably, despite high density, polymorphic markers coverage was incomplete in some genomic regions. As such, 28 and 37 linkage groups were obtained in POP1 and POP2, respectively corresponding to the 20 soybean chromosomes. Using RRW, one QTL was identified in POP1 on Chromosome 20 that explained 12.7–13.3% of phenotypic variation. The desirable allele of this QTL was from ‘E05226-T’. Another QTL was found in POP2 on Chromosome 11. It explained 15.4% of the phenotypic variation and the desirable allele was from ‘E09088’. However, no QTL were identified using RWI in either population. These results supported that RRW was more suitable to be used to evaluate P. irregulare tolerance in soybean.
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