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Genome‐Wide Association Study of Brown Stem Rot Resistance in Soybean across Multiple Populations
Author(s) -
Rincker Keith,
Lipka Alexander E.,
Diers Brian W.
Publication year - 2016
Publication title -
the plant genome
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 41
ISSN - 1940-3372
DOI - 10.3835/plantgenome2015.08.0064
Subject(s) - biology , genome wide association study , genetics , single nucleotide polymorphism , association mapping , genome , plant disease resistance , chromosome , gene , selection (genetic algorithm) , quantitative trait locus , allele , resistance (ecology) , genotype , agronomy , artificial intelligence , computer science
Genetic resistance to brown stem rot (BSR) of soybean [ Glycine max (L.) Merr.], caused by Cadophora gregata (Allington & D.W. Chamb.) T.C. Harr. & McNew, has been identified and mapped with biparental populations. Although nearly 400 accessions have been identified with BSR resistance, this trait has been mapped in only 12 sources, and just two, PI84946‐2 and PI88788, have been used to develop BSR resistant cultivars. Thus, there is a serious need to improve our knowledge of the genetic basis of BSR resistance in soybean so that resistance genes in cultivars can be diversified and markers close to resistance genes can be identified and used in marker‐assisted selection (MAS). To this end, we conducted a genome‐wide association study (GWAS) to identify novel genomic loci associated with BSR resistance and to gain further insight into a previously reported chromosome 16 region containing BSR resistance ( Rbs ) genes. A total of 52,041 single‐nucleotide polymorphisms (SNPs) were tested for association with BSR in a set of 4735 accessions from four diversity panels evaluated for resistance from 1989 to 2003. Using a unified mixed linear model and stepwise model selection, we refined the signals within the Rbs interval on chromosome 16 by finding associations that explain a substantial proportion of the total variation of BSR resistance. In combination with significant GWAS signals found elsewhere in the genome, our study will aid efforts to improve BSR resistance by providing new targets for MAS.

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