Theoretical and Applied Genetics

, Volume 102, Issue 2, pp 187–192

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

Authors

  • M. J. Iqbal
    • Center for Excellence in Soybean Research, Department of Plant, Soil and General Agriculture, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA e-mail: mjiqbal@siu.edu Fax: (618) 453–7457
  • K. Meksem
    • Center for Excellence in Soybean Research, Department of Plant, Soil and General Agriculture, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA e-mail: mjiqbal@siu.edu Fax: (618) 453–7457
  • V. N. Njiti
    • Center for Excellence in Soybean Research, Department of Plant, Soil and General Agriculture, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA e-mail: mjiqbal@siu.edu Fax: (618) 453–7457
  • My. A. Kassem
    • Center for Excellence in Soybean Research, Department of Plant, Soil and General Agriculture, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA e-mail: mjiqbal@siu.edu Fax: (618) 453–7457
  • D. A. Lightfoot
    • Center for Excellence in Soybean Research, Department of Plant, Soil and General Agriculture, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA e-mail: mjiqbal@siu.edu Fax: (618) 453–7457
Original Paper

DOI: 10.1007/s001220051634

Cite this article as:
Iqbal, M., Meksem, K., Njiti, V. et al. Theor Appl Genet (2001) 102: 187. doi:10.1007/s001220051634

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 quantitatively 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, R2= 24.1%), BARC-Satt309 (P = 0.0001, R2 = 16.3), BARC-Satt570 (P = 0.0001, R2 = 19.2%) and a random amplified polymorphic DNA (RAPD) marker OEO21000 (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 disease incidence (DI). All the QTLs on LG G derived the beneficial allele from Forrest. Two QTLs, BARC-Satt371 (P = 0.0019, R2 = 12%) on LG C2 (previously reported) and BARC-Satt354 (P = 0.0015, R2 = 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 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.

Keywords Soybean sudden-death syndrome (SDS)Quantitative trait lociMicrosatellite markersRecombinant inbred lines

Copyright information

© Springer-Verlag Berlin Heidelberg 2001