Soybean (Glycine max (L.) Merr.) cultivars differ in their resistance to sudden death syndrome (SDS), caused by Fusarium virguliforme (Aoki). Breeding for improving SDS response has been challenging, due to the large number of known resistance loci (more than 43) and interactions among them. The aims here were to compare the inheritance of resistance to SDS in a near isogenic line (NIL) population that was fixed for 91.5% of the genome but appeared to segregated at loci underlying partial resistance to SDS; to examine the interaction with the loci; and to identify regions containing candidate genes underlying QTL. Used were; a NIL population derived from residual heterozygosity in an F5:9 recombinant inbred line EF60 (lines 1-40). The SDS disease index (DX) data were from two locations but two different years. There were 4 of 400 microsatellite and 456 of 5,361 SNP markers tested that were polymorphic (8-10%). The SNPs clustered into 23 genomic regions. Significantly associated with resistance to SDS (0.005 < P > 0.0001) were regions from 2,788 Kbp to 8,938 Kbp on chromosome (Chr.) 18 and 33,100 Kbp to 34,943 Kbp on Chr. 20. The marker to trait association values suggested that the two closely linked loci on Chr. 18 were really three loci (cqRfs1, cqRfs, and now Rfs19). They were clustered within 20 cM of the rhg1 locus underlying resistance to soybean cyst nematode (SCN; HgType 7). An epistatic interaction between the Chr18 loci and the Chr 20 locus were inferred. Therefore, QTL for resistance to SDS were shown to be both internally complex and interacting.



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