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This article in TPG

  1. Vol. 10 No. 2
    unlockOPEN ACCESS
     
    Received: June 08, 2016
    Accepted: Feb 15, 2017
    Published: July 13, 2017


    * Corresponding author(s): jspecht1@unl.edu
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doi:10.3835/plantgenome2016.06.0054

Genome-wide Association Mapping of Qualitatively Inherited Traits in a Germplasm Collection

  1. Nonoy B. Bandilloa,
  2. Aaron J. Lorenza,
  3. George L. Graefa,
  4. Diego Jarquina,
  5. David L. Hytena,
  6. Randall L Nelsonb and
  7. James E. Specht *a
  1. a Dep. of Agronomy & Horticulture, Univ. of Nebraska-Lincoln, Keim Hall Lincoln, NE 68583-0915
    b USDA-ARS, Soybean/Maize Germplasm, Pathology, and Genetics Research Unit and Dep. of Crop Sciences, Univ. of Illinois, 1101 West Peabody Drive, Urbana, IL 61801-0000
Core Ideas:
  • Genome-wide association (GWA) is usually aimed at quantitative (but not so much at qualitative) traits.
  • Germplasm collections have extensive data on qualitatively inherited descriptor traits.
  • Positional location of classical genes is lacking in most crop genome sequence maps.
  • Genome-wide association easily generates high-resolution genome sequence map positions for classical loci.
  • Genome-wide association-based gene positions are attainable even for traits governed by digenic epistasis.

Abstract

Genome-wide association (GWA) has been used as a tool for dissecting the genetic architecture of quantitatively inherited traits. We demonstrate here that GWA can also be highly useful for detecting many major genes governing categorically defined phenotype variants that exist for qualitatively inherited traits in a germplasm collection. Genome-wide association mapping was applied to categorical phenotypic data available for 10 descriptive traits in a collection of ∼13,000 soybean [Glycine max (L.) Merr.] accessions that had been genotyped with a 50,000 single nucleotide polymorphism (SNP) chip. A GWA on a panel of accessions of this magnitude can offer substantial statistical power and mapping resolution, and we found that GWA mapping resulted in the identification of strong SNP signals for 24 classical genes as well as several heretofore unknown genes controlling the phenotypic variants in those traits. Because some of these genes had been cloned, we were able to show that the narrow GWA mapping SNP signal regions that we detected for the phenotypic variants had chromosomal bp spans that, with just one exception, overlapped the bp region of the cloned genes, despite local variation in SNP number and nonuniform SNP distribution in the chip set.

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