Genome-Wide Association and Epistasis Studies Unravel the Genetic Architecture of Sudden Death Syndrome Resistance in Soybean

Soybean [Glycine max (L.) Merr.] is an economically important crop grown worldwide. Sudden death syndrome (SDS), caused by Fusarium virguliforme, is one of the top yield-limiting diseases in soybean. However, the genetic basis, especially the epistatic interactions, of SDS resistance is still unclear. To better understand the genetic architecture of soybean SDS resistance, genome-wide association and epistasis studies were conducted using a population of 214 germplasm accessions and 31,914 single nucleotide polymorphisms (SNPs) from SoySNP50K Illumina Infinium BeadChip.

Twelve loci and 12 SNP-SNP interactions associated with SDS resistance were identified at different time-points after inoculation. These additive and epistatic loci together explained 24-52% of phenotypic variances. Disease-resistant, pathogenesis-related and chitin- and wound-responsive genes were identified in the proximity of peak SNPs, including the gene stress-induced receptor-like kinase gene 1 (SIK1) that is pinpointed by a trait-associated non-synonymous SNP and encodes a Leucine-rich repeat containing protein. We report that the proportion of phenotypic variance explained by identified loci can be considerably improved by taking the epistatic effects into account.

This study shows the necessity of involving epistatic effects in soybean SDS resistance breeding using marker-assisted and genomic selection approaches. Based on our findings we proposed a model of soybean root defense against the SDS pathogen. Our results facilitate the identification of the molecular mechanism underlying SDS resistance in soybean, and lay a genetic basis for soybean SDS resistance improvement through breeding strategies built upon additive and epistatic effects.