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Inheritance of Partial Resistance to Sclerotinia Stem Rot in Soybean


This article in CS

  1. Vol. 40 No. 1, p. 55-61
    Received: Aug 13, 1998

    * Corresponding author(s): bdiers@uiuc.edu
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  1. H. S. Kima and
  2. B. W. Diers *b
  1. a Upland Crop Division, National Crop Exp. Stn., Suwon 441-100, South Korea
    b Dep. of Crop Sciences, University of Illinois, Urbana, IL 61801 USA


Little is known about the inheritance of partial resistance in soybean [Glycine max (L.) Merr.] to sclerotinia stem rot, caused by the fungal pathogen Sclerotinia sclerotiorum (Lib.) de Bary. This information would be useful to soybean breeders who are developing cultivars with resistance to sclerotinia stem rot. Our objectives were to study the inheritance of partial resistance to sclerotinia stem rot and to present the initial results from mapping quantitative trait loci (QTL) that confer this resistance. The research was conducted by testing 152 F3-derived lines from a cross between a partially resistant cultivar, Novartis Seeds S19-90 (formerly Northrup King), and a susceptible cultivar, Williams 82, for resistance to sclerotinia stem rot and agronomic traits at two Michigan locations in each of 2 yr. These lines were also evaluated for 123 genetic markers to map resistance genes. The resistance of the lines, measured with a disease severity index (DSI), was normally distributed across environments. Significant (P < 0.05) genotypic variation, genotype × location, and genotype × year interactions were observed for DSI. The broad-sense heritability estimate for DSI across both locations and years was 0.59. More severe disease was significantly correlated with greater lodging, later date of maturity, later R1 date, and greater plant height. Three QTL, explaining 10, 9, and 8% of the variability for DSI across environments, were mapped with genetic markers. Two of these QTL were also significantly associated with disease escape mechanisms such as plant height, lodging, and date of flowering. The other QTL was not significantly associated with escape mechanisms and may map one or more genes involved in physiological resistance to the disease.

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