|WEN, ZIXIANG - Michigan State University
|TAN, RUIJUAN - Michigan State University
|YUAN, JIAZHENG - Michigan State University
|BALES, CARMILLE - Michigan State University
|DU, WENYAN - Michigan State University
|ZHANG, SHICHEN - Michigan State University
|CHILVERS, MARTING - Michigan State University
|SCHMIDT, CATHY - Southern Illinois University
|KULL, LINDA - University Of Illinois
|WANG, DECHUN - Michigan State University
Submitted to: BMC Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/18/2014
Publication Date: 9/1/2014
Citation: Wen, Z., Tan, R., Yuan, J., Bales, C., Du, W., Zhang, S., Chilvers, M., Schmidt, C., Song, Q., Cregan, P.B., Kull, L., Wang, D. 2014. Genome-wide association mapping of quantitative resistance to sudden death syndrome in soybean. Biomed Central (BMC) Genomics. 15:809.
Interpretive Summary: Sudden death syndrome (SDS) caused by the fungal pathogen Fusarium virguliforme is a serious threat to U.S. soybean production. In order to determine the genetics of resistance to SDS a technique called genetic association analysis was used to analyze different sets of soybean accessions from the USDA Soybean Germplasm Collection consisting of 392 and 300 unique soybean accessions. Both sets of accessions were evaluated for resistance to SDS and were also evaluated with a large number of single nucleotide polymorphism (SNP) DNA markers. The resulting genetic association analysis of the SDS resistance assessment and the SNP DNA markers detected 20 genome positions with genes controlling resistance to SDS. Seven of these genome positions had previously been determined to have genes controlling resistance to SDS. One of the seven positions previously determined to contain a gene providing SDS resistance contained the important SDS resistance gene GmRLK18-1. The identification of the many potential genes controlling SDS resistance should allow marker-assisted selections in soybean for increased resistance to SDS.
Technical Abstract: Sudden death syndrome (SDS) is a serious threat to soybean production that can be controlled by host plant resistance. To dissect the genetic architecture of quantitative resistance to the disease in soybean, two independent association panels of soybean elite cultivar, consisting of 392 and 300 unique accessions, were evaluated for resistance to SDS in multi-environments. Genome-wide association mapping was conducted by genotyping 52,041 and 5,361 SNPs variants across the two association panels respectively. A total of 20 loci underling SDS resistance were identified in the two independent studies, including 7 loci localized in previously mapped QTL intervals and 13 novel loci. One strong peak of association on chromosome 18, associated with all disease assessment criteria across the two panels, spanned a physical region of 1.2 Mb around previously cloned SDS resistance gene (GmRLK18-1), and there was an additional variants independently associated with SDS resistance in this genomic region. Other peak SNPs were within or close to sequences annotated as homologous to genes previously shown to be involved in plant disease resistance. Peak SNPs at the identified loci could explain approximately 54.5% of the phenotypic variance on average measured by different disease assessment criteria. The identification of such associations may provide substantial insight into soybean resistance to SDS and may also facilitate marker-assisted selections in soybean.