Microsatellite markers identify three additional quantitative trait loci for resistance to soybean sudden-death syndrome (SDS) in Essex x Forrest RILs

Resistance to the sudden-death syndrome (SDS) of soybean (Glycine max L. Me rr.), caused by Fusarium solani f. sp. glycines, is controlled by a number of quantitatively inherited loci (QTLs). Forrest showed a strong field resi stance to SDS while Essex is susceptible to SDS. A population of 100 recomb inant inbred lines (RILs) derived from a cross of Essex x Forrest was used to map the loci effecting resistance to SDS using phenotypic data obtained from six environments. Six loci involved in resistance to SDS were identifi ed in this population. Four of the QTLs identified by BARC-Satt214 (P = 0.0 001, R-2= 24.1%), BARC-Satt309 (P = 0.0001, R-2 = 16.3), BARC-Satt570 (P = 0.0001, R-2 = 19.2%) and a random amplified polymorphic DNA (RAPD) marker O EO2(1000) (P = 0.0031, R-2=12.6) were located on linkage group (LG) G (Satt 309 and OEO2(1000) were previously reported). Jointly the four QTLs on LG G explained 50% of the variation in SDS disease incidence (DI). All the QTLs on LG G derived the beneficial allele from Forrest. Two QTLs, BARC-Satt371 (P = 0.0019, R-2 = 12%) on LG C2 (previously reported) and BARC-Satt354 (P = 0.0015, R-2 = 11.5%) on LG I, derived their beneficial allele from Essex and jointly explained about 40% of the variation in SDS DI. Two-way and mu lti-way interactions indicated that gene action was additive among the loci underlying resistance to SDS. These results suggest that cultivars with du rable resistance to SDS can be developed via gene pyramiding.