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Olney Central College, Olney IL 62450
Dept. of Plant and Soil Science, Molecular Science Program, Southern Illinois Univ., Carbonadale, IL 62091
* Corresponding author (ga4082{at}siucvmb.siu.edu).
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.
Received for publication March 19, 1995.
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