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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #314224
Title: Genetic architecture of cyst nematode resistance revealed by genome-wide association study in soybean

Author
item VUONG, T - University Of Missouri
item SONAH, H - University Of Missouri
item MEINHARDT, C - University Of Missouri
item DESHMUKH, R - University Of Missouri
item KADAM, S - University Of Missouri
item Nelson, Randall
item SHANNON, J - University Of Missouri
item NGUYEN, H - University Of Missouri

Submitted to: BMC Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/3/2015
Publication Date: 8/12/2015
Citation: Vuong, T.D., Sonah, H., Meinhardt, C.G., Deshmukh, R., Kadam, S., Nelson, R.L., Shannon, J.G., Nguyen, H.T. 2015. Genetic architecture of cyst nematode resistance revealed by genome-wide association study in soybean. Biomed Central (BMC) Genomics. 16:593.

Interpretive Summary: The genetic control of complex traits such as resistance to soybean cyst nematode (SCN) has generally been characterize with genetic mapping in populations created by crossing two parents that differ in their resistance to SCN. This approach has successfully mapped a large number of genomic regions associated with SCN resistance, but it captures only a limited amount of the diversity that exists in the parental lines and cannot precisely locate the position of the resistance genes on the appropriate chromosome. In this study, a genome-wide association study (GWAS) was performed using a diverse set of 553 soybean introductions from the USDA Soybean Germplasm Collection. This research associates the known SCN resistance classification of each soybean lines with over 45,000 DNA markers to precisely locate the genes conditioning SCN resistance. We identified SCN resistance on 14 different chromosomes. Our results confirmed six genomic locations associated with SCN resistance that were previously mapped using bi-parental populations and eight new locations. This research demonstrates that GWAS is an effective strategy for identifying complex traits such as SCN resistance in soybean and for more precising locating the genes responsible for that resistance. These results are of use to all scientist interested in SCN resistance and to plant breeders and geneticists who would use GWAS in their research.

Technical Abstract: Bi-parental mapping populations have been commonly utilized to identify and characterize quantitative trait loci (QTL) controlling resistance to soybean cyst nematode (SCN, Heterodera glycines Ichinohe). Although this approach successfully mapped a large number of SCN resistance QTL, it captures only limited allelic diversity that exists in parental lines, and it also has limitations for genomic resolution. In this study, a genome-wide association study (GWAS) was performed using a diverse set of 553 soybean plant introductions (PIs) belonging to maturity groups from III to V to detect QTL/genes associated with SCN resistance to HG Type 0. Over 45,000 single nucleotide polymorphism (SNP) markers generated by the SoySNP50K iSelect BeadChip (http//www.soybase.org) were utilized for analysis. GWAS identified 14 loci distributed over different chromosomes comprising 60 SNPs significantly associated with SCN resistance. Results also confirmed six QTL that were previously mapped using bi-parental populations, including the rhg1 and Rhg4 loci. GWAS identified eight novel QTL, including QTL on chromosome 10, which we have previously mapped by using a bi-parental population. In addition to the known loci for four simple traits, such as seed coat color, flower color, pubescence color, and stem growth habit, two traits, like lodging and pod shattering, having moderately complex inheritance have been confirmed with great precision by GWAS. The study showed that GWAS can be employed as an effective strategy for identifying complex traits in soybean and for narrowing GWAS-defined genomic regions, which facilitates positional cloning of the causal gene(s).