Sudden death syndrome (SDS), caused by the soil-borne fungus Fusarium virguliforme, is a devastating disease of soybean and has been found in most soybean growing regions of the United States. Use of SDS resistant cultivars is the most cost-efficient method to manage this disease. Dissecting the genetic architecture of SDS resistance is essential for soybean breeding. In this study, two recombinant inbred line populations with genotypes obtained from Infinium SoySNP6K BeadChip were employed to 1) identify loci underlying the root and foliar resistance to SDS; 2) investigate the effect of epistatic interaction on SDS resistance; and 3) examine the relationship among F. virguliforme colonization in root, foliar damage, and yield. In the population generated from the cross GD2422 × LD01-5907, four quantitative trait loci (QTLs) were identified and mapped on Chromosomes 4, 8, 12, and 18. The resistant parent, LD01-5907, conferred the resistance alleles for the QTLs on Chromosomes 8 and 18, while the susceptible parent, GD2422, provided the resistance alleles for the QTLs on Chromosomes 4 and 12. The minor QTL mapped on Chromosome 12 is novel. The QTLs identified on Chromosomes 8 and 18 overlapped with two loci underlying soybean cyst nematode (SCN) resistance, Rhg4 and Rhg1, respectively. A significant epistatic interaction between the two QTLs on Chromosomes 8 and 18 was detected by disease incidence across two years. Individual effects of these two QTLs together with their interaction effect explained around 70% of phenotypic variance. The epistatic interaction was confirmed by field performance across multiple years at the genotypic group, progeny line, and single plant levels. In addition, the resistance alleles at the QTLs on Chromosomes 8 and 18 showed recessive inheritance.In the population derived from the cross U01-390489 × E07080, a weak positive correlation was observed between the F. virguliforme content in root and foliar damage. Compared to F. virguliforme content, the foliar damage showed stronger negative correlation with plot yield with the disease index showing the highest correlation coefficient. Twelve loci associated with foliar resistance were identified, and four of them were detected by multiple foliar-damage related parameters across several environments. These loci were mapped on Chromosomes 6, 9, and 18. In contrast, only one QTL was identified for resistance to F. virguliforme content and mapped on Chromosome 18. It overlapped with the QTL identified by disease index in the same environment. Given that the stability of identified QTLs across environments and higher correlation with plot yield, foliar symptom related parameters, especially disease index, were more valuable for SDS resistance breeding. The molecular markers associated with the identified QTLs and other information present in this research will aid the marker-assisted selection for resistance to SDS in soybean breeding.
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