|TAN, RUIJUAN - Michigan State University|
|WEN, ZIXIANG - Michigan State University|
|BOYSE, JOHN - Michigan State University|
|CHILVERS, MARTIN - Michigan State University|
|WANG, DECHUN - Michigan State University|
Submitted to: Crop Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/12/2021
Publication Date: 2/2/2022
Citation: Collins, P.J., Tan, R., Wen, Z., Boyse, J., Chilvers, M.I., Wang, D. 2022. Genetic mapping of host resistance to soybean sudden death syndrome. Crop Science. https://doi.org/10.1002/csc2.20689.
Interpretive Summary: Soybean sudden death syndrome (SDS) is caused by a fungus in the soil. Breeding programs are developing soybean varieties which are resistant to this disease. The breeder identified resistant lines and used those lines as parents to identify genes for resistance to SDS. Three breeding populations, which were crosses between SDS resistant and SDS susceptible varieties, were evaluated in a field infested with the SDS pathogen. These populations were also genotyped using molecular markers (a similar technology as is used by 23 and Me). A correlation of the genetic marker data with the field data allowed for the identifications of regions of the soybean genome which were associated with resistance. The results revealed two new genes for SDS resistance and confirmed the identification of a major resistance gene indicated by previous studies that is also associated with resistance to soybean cyst nematode, suggesting a connection between fungal and nematode infection.
Technical Abstract: Soybean sudden death syndrome (SDS) is a disease caused by a soil-borne fungus, Fusarium virguliforme. Many genetic studies have attempted to identify genes responsible for the quantitative host resistance to SDS. Three recombinant inbred line (RIL) populations were evaluated for foliar SDS resistance at a naturally infested field site in Decatur, MI during the 2014 and 2015 growing seasons. Lines were evaluated for disease severity (DS) on a 1-9 scale, disease incidence (DI) as an estimate of the percentage of plants with symptoms per plot, and disease index (DX) as a metric which integrates DS and DI. Phenotypic data was spatially adjusted to account for uneven pathogen distribution in the naturally infested field. A subset of RILs from each population were genotyped with the SoySNP6K Illumina Infinium BeadChip. Linkage maps unique to each population were constructed using JoinMap ver. 2. Composite interval mapping was performed using WinQTLCartographer ver. 2.5. Three quantitative trait loci (QTL) were identified across multiple years and/or populations. One QTL on Chromosome Gm10 appeared to be colocalized with the E2 maturity locus. Kompetitive Allele Specific Primers (KASP from LGC Genomics) were developed to identify recombination events within this QTL region in the selfed progeny of a residual heterozygous line (RHL). The RHL progeny with recombination events were evaluated at the Decatur, MI fieldsite to narrow the QTL region responsible for SDS resistance. Another QTL identified was on Chromosome Gm18, in a region which has been demonstrated to provide SCN and SDS resistance in many studies (rhg1/Rfs2).