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Dep. of Plant Soil and General Agriculture, Center for Excellence in Soybean Research, Teaching and Outreach, Southern Illinois University, Carbondale, IL 62901.
Corresponding author (ga4082{at}siu.edu).
DNA markers for genes conditioning resistance to soybean [Glycine max (L.) Merr.] root infection by [Fusarium solani (Mart.) Sacc. f. sp. glycine (Burk.)] (Rfs1), sudden death syndrome (SDS), and soybean cyst nematode (SCN; Heterodera glycines Ichinohe; Rhg4 and rhg1) were previously identified in ‘Essex’ x ‘Forrest’. This study tests the effectiveness of those markers in selecting for disease resistance among recombinant inbred lines from ‘Flyer’ x ‘Hartwig’. A total of 535 among 739 lines were scored by two markers, providing four genotypes. A stratified random sample of 50 lines was evaluated for SDS by F. solani root infection severity at two locations and SCN race 3 index of parasitism in the greenhouse. Selection with BLT65 identified 281 among 671 lines with the genomic region that underlies Rhg4-derived SCN resistance. Selection with Satt038 identified 230 among 613 lines containing the genomic region that underlies resistance to SDS (rfs1) and rhg1 -derived SCN resistance. A total of 93 out of 535 lines had genomic regions that underlie resistance to both SDS and SCN in Essex x Forrest. Segregation of both markers was not random (P 
0.05). Infection severity means for genotypes with the Hartwig allele at Satt038 (28–29%) were lower (P = 0.0001, R2 = 28%) than with the Flyer allele (31–42%); irrespective of maturity group. BLT65 was not associated with infection severity. Mean SCN index of parasitism was lower (P 0.05) only for genotypes carrying the Hartwig allele at both Satt038 and BLT65. Therefore, alleles conferring resistance to SDS and SCN in Essex x Forrest are transferable to other populations.
Received for publication June 22, 1998.
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