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Crop Science Abstract -

Quantitative Trait Loci Controlling Resistance to Gray Leaf Spot in Maize


This article in CS

  1. Vol. 33 No. 4, p. 838-847
    Received: Feb 24, 1992

    * Corresponding author(s):
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  1. D. M. Bubeck ,
  2. M. M. Goodman,
  3. W. D. Beavis and
  4. D. Grant
  1. N orthrup King Co., 317 St., Stanton, MN 55018-4308
    C rop Sci. Dep., Box 7620, North Carolina St. Univ., Raleigh, NC 27695
    D ep. of Data Management
    D ep. of Biotechnology, Pioneer Hi-Breed International, Inc., 7250 N.W. 62nd Ave., Johnston, IA 50131



Gray leaf spot (GLS) (caused Cercospora zeae-maydis Theon & Daniels) is a fungal disease of the maize (Zea mays L.) that can cause significant grain yield reductions. Quantitative resistance to GLS does exist; therefore, one method of controlling the disease is to develop hybrids with genetic resistance. The objective of this study was to identify quantitative trait loci (QTL) and type-of-gene action for GLS resistance in segregating families of three single-cross populations of maize using restriction fragment length polymorphisms (RFLPs). We also attempted to determine the consistency of QTL over environments and populations. Population 1 (POP1) consisted of 139 F2:3 families evaluated in three environments. Population 2 (POP2) consisted 193 F2:3 families and Population 3 (POP3) had 144 F2:3 families; POP2 and POP3 were considered as replicate populations evaluated in separate environments. Families were rated for GLS on a plot basis by a scale of 1 (susceptible) to 9 (resistant), and ratings were taken at 5- to 18-d intervals in each environment. The QTL were identified on the basis of marker associations with GLS means over all ratings taken in an environment, as well as a GLS mean over environments for POP1 and over POP2 and POP3 for the replicate populations. Based on single-factor ANOVA, detectable individual markers accounted for 4 to 26% of the phenotypic variation. The QTL associated with GLS were inconsistent over environments, but the cause of these differences could not be determined. One region on chromosome 2 was associated with GLS resistance in POP1, POP2, and POP3. Additive gene action was displayed for nearly all markers associated with resistance.

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