Genome‐wide association and epistasis studies unravel the genetic architecture of sudden death syndrome resistance in soybean

• Published in: The Plant journal : for cell and molecular biology Vol. 84; no. 6; pp. 1124 - 1136
• Main Authors: Zhang, Jiaoping, Singh, Arti, Mueller, Daren S., Singh, Asheesh K.
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01.12.2015
• Subjects: Botany; Epistasis, Genetic - physiology; epistatic interaction; Fusarium; Genetic Markers; Genetic Variation; Genome-Wide Association Study; Genomics; Glycine max (L.) Merr; Glycine max - genetics; Kinases; Linkage Disequilibrium; plant defense; Plant Diseases - immunology; Plant Diseases - microbiology; Plant Proteins - genetics; Plant Proteins - metabolism; Plant resistance; Polymorphism; SNP–SNP interaction; Soybeans; sudden death syndrome; epistatic interaction; plant defense; Glycine max (L.) Merr; sudden death syndrome; genome-wide association study; SNP-SNP interaction; linkage disequilibrium
• ISSN: 0960-7412; 1365-313X
• DOI: 10.1111/tpj.13069

Summary Soybean [Glycine max (L.) Merr.] is an economically important crop that is grown worldwide. Sudden death syndrome (SDS), caused by Fusarium virguliforme, is one of the top yield‐limiting diseases in soybean. However, the genetic basis of SDS resistance, especially with respect to epistatic interactions, is still unclear. To better understand the genetic architecture of soybean SDS resistance, genome‐wide association and epistasis studies were performed using a population of 214 germplasm accessions and 31 914 SNPs from the SoySNP50K Illumina Infinium BeadChip. Twelve loci and 12 SNP–SNP interactions associated with SDS resistance were identified at various time points after inoculation. These additive and epistatic loci together explained 24–52% of the phenotypic variance. Disease‐resistant, pathogenesis‐related and chitin‐ and wound‐responsive genes were identified in the proximity of peak SNPs, including stress‐induced receptor‐like kinase gene 1 (SIK1), which is pinpointed by a trait‐associated SNP and encodes a leucine‐rich repeat‐containing protein. We report that the proportion of phenotypic variance explained by identified loci may be considerably improved by taking epistatic effects into account. This study shows the necessity of considering epistatic effects in soybean SDS resistance breeding using marker‐assisted and genomic selection approaches. Based on our findings, we propose a model for soybean root defense against the SDS pathogen. Our results facilitate identification of the molecular mechanism underlying SDS resistance in soybean, and provide a genetic basis for improvement of soybean SDS resistance through breeding strategies based on additive and epistatic effects. Significance Statement We report 12 additive effect loci and 12 epistatic interactions associated with resistance to sudden death syndrome in soybean; and pinpoint a trait‐associated single nucleotide polymorphism in SIK1, encoding a leucine‐rich receptor kinase.