Sudden death syndrome (SDS) is a fungal disease of soybean [Glycine max (L.) Merr.], caused by Fusarium solani (Mart.) Sacc. f. sp. phaseoli (Burk.) Snyd. & Hans., type A (FSA), that reduces crop yields in the USA. Quantitative partial resistance to SDS does exist; therefore, one method of controlling the disease is to select cultivars with genetic resistance. The objective of this study was to use molecular markers to identify and locate alleles of chromosomal segments associated with field resistance to SDS in adapted soybean genotypes. Seventy polymorphic DNA markers were compared with SDS response among 100 F5:9 recombinant inbred lines derived from a cross between SDS‐resistant ‘Forrest’ and SDS‐susceptible ‘Essex’. SDS disease incidence (D1), disease severity (DS), and yield were determined in replicated, FSA‐infested test sites during 4 yr encompassing five locations with recombinant inbred lines from the F5:7 to F5‐11.Two separate chromosomal segments identified by two RAPD markers, OOO5250 and OC0l650, were found to be associated with mean SDS response across five locations as well as within each of the five locations. These two quantitative trait loci (QTL) jointly accounted for 34% of total phenotypic variability in mean D1. OCOl650 was significantly associated with mean DS and yield and was putatively assigned to linkage group N. The beneficial allele was derived from the resistant parent Forrest. OO05250 was not significantly associated with mean DS or yield and was putatively assigned to linkage group C. The beneficial allele was derived from the susceptible parent Essex. Molecular markers can be used to define alleles of chromosomal segments conferring resistance to SDS in several environments and may allow efficient selection of resistant genotypes with good yield potential for FSA‐infested fields.

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Coinheritance of field resistance of soybean [Glycine max (L.) Merr.] to sudden death syndrome (SDS) [caused by the fungus Fusarium solani (Mart.) Sacc. f. sp. phaseoli (Burk.) Snyd. & Hans.] and soybean cyst nematode (SCN) race 3 (caused by Heterodera glycines Ichinohe) sometimes occurs in crosses among adapted cultivars. Our objective was to characterize the loci underlying this coinheritance. One hundred thirty DNA markers were compared with SDS disease response and SCN score among 100 recombinant inbred lines (RILs) derived from a cross between SDS and SCN resistant ‘Forrest’ and SDS and SCN susceptible ‘Essex’. SDS disease incidence (DI) was determined in replicated sites during 4 yr encompassing five locations. The SCN score was determined in the greenhouse from naturally infested field soil samples. Two separate genomic regions identified by random amplified polymorphic DNA (RAPD) markers OI03450 and OW15400 were associated with mean SCN score (P = 0.0001) and jointly accounted for about 47% of variability in SCN score. OI03450 identified a QTL for resistance to SCN (R2 = 14%) within a genomic region that was strongly associated with SDS DI (R2 = 20%), partly explaining the coinheritance of the two traits. This locus could be assigned to the region of linkage group G already known to encompass the major SCN resistance locus.

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