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

Abstract

Resistance to the sudden-death syndrome (SDS) of soybean (Glycine max L. Merr.), caused by Fusarium solani f. sp. glycines, is controlled by a number of quantita- tively inherited loci (QTLs). Forrest showed a strong field resistance to SDS while Essex is susceptible to SDS. A population of 100 recombinant inbred lines (RILs) derived from a cross of Essex × 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 identified in this population. Four of the QTLs identified by BARC-Satt214 (P = 0.0001, R 2 = 24.1%), BARC-Satt309 (P = 0.0001, R2 = 16.3), BARC-Satt570 (P = 0.0001, R 2 = 19.2%) and a random amplified poly- morphic DNA (RAPD) marker OEO2 1000 (P = 0.0031, R2=12.6) were located on linkage group (LG) G (Satt309 and OEO21000 were previously reported). Jointly the four QTLs on LG G explained 50% of the variation in SDS dis- ease 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, R2 = 11.5%) on LG I, de- rived their beneficial allele from Essex and jointly ex- plained about 40% of the variation in SDS DI. Two-way and multi-way interactions indicated that gene action was additive among the loci underlying resistance to SDS. These results suggest that cultivars with durable resistance to SDS can be developed via gene pyramiding.