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This article in CS

  1. Vol. 36 No. 5, p. 1344-1351
     
    Received: Sept 21, 1995
    Published: Sept, 1996


    * Corresponding author(s): pmiklas@tricity.wsu.edu
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doi:10.2135/cropsci1996.0011183X003600050044x

Selective Mapping of QTL Conditioning Disease Resistance in Common Bean

  1. Phillip N. Miklas ,
  2. Elizabeth Johnson,
  3. Valerie Stone,
  4. James S. Beaver,
  5. Carlos Montoya and
  6. Mildred Zapata
  1. U SDA-ARS-IAREC, 24106 N. Bunn Rd., Prosser, WA 99350-9687
    C rop Science Department, North Carolina State Univ., Raleigh, NC 27695
    U SDA-ARS-TARS, P.O. Box 70, Mayagüez, Puerto Rico, 00681
    D ep. of Agronomy and Soils
    I CA, A.A. 233, Palmira, Colombia
    D ep. of Crop Protection, Univ. of Puerto Rico, Mayagüez, Puerto Rico 00681

Abstract

Abstract

Genetic markers linked with quantitative trait loci (QTL) may enable indirect selection of complex disease resistance. Construction of separate linkage maps to identify QTL for each complex disease resistance trait of common bean (Phaseolus vulgaris L.) is unfeasible, however. We investigated whether selective mapping could be used to hasten identification of random amplified polymorphic DNA (RAPD) associated with QTL conditioning bean golden mosaic virus (BGMV) or common bacterial blight (CBB) resistance. The mapping population (‘Dorado’ × XAN 176) consisted of 79 F5:7 recombinant inbred lines. A bulked segregant analysis (BSA) of as few as three individuals and selective genotyping was used. The 101 RAPDs identified between the parents were tested across resistant vs. susceptible bulks for BGMV reaction, combined greenhouse (leaf) and field reactions to CBB, and pod (greenhouse) reaction to CBB. Fourteen of 22 RAPDs selectively mapped because they cosegregated among lines within bulks, were linked with seven of the nine QTL conditioning resistance as identified by QTL mapping using all 101 RAPDs. The two QTL not identified by this approach had minor effects. BSA and selective genotyping required only about one-third the cost and labor of completely classifying the whole population with each marker and was similarly effective for identifying RAPD markers associated with major-effect QTL that condition disease resistance in common bean. Two-locus models (R2), for select environments, explained 60% of the phenotypic variation in BGMV reaction, and 65, 58, and 46% of the phenotypic variation in greenhouse-leaf, -pod, and field reactions to CBB. Repulsion linkages between QTL for BGMV and CBB may complicate the combination of resistance alleles for these two traits.

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