Genotyping-by-sequencing markers facilitate the identification of quantitative trait loci controlling resistance to Penicillium expansum in Malus sieversii

PLoS One. 2017 Mar 3;12(3):e0172949. doi: 10.1371/journal.pone.0172949. eCollection 2017.

Abstract

Blue mold caused by Penicillium expansum is the most important postharvest disease of apple worldwide and results in significant financial losses. There are no defined sources of resistance to blue mold in domesticated apple. However, resistance has been described in wild Malus sieversii accessions, including plant introduction (PI)613981. The objective of the present study was to identify the genetic loci controlling resistance to blue mold in this accession. We describe the first quantitative trait loci (QTL) reported in the Rosaceae tribe Maleae conditioning resistance to P. expansum on genetic linkage group 3 (qM-Pe3.1) and linkage group 10 (qM-Pe10.1). These loci were identified in a M.× domestica 'Royal Gala' X M. sieversii PI613981 family (GMAL4593) based on blue mold lesion diameter seven days post-inoculation in mature, wounded apple fruit inoculated with P. expansum. Phenotypic analyses were conducted in 169 progeny over a four year period. PI613981 was the source of the resistance allele for qM-Pe3.1, a QTL with a major effect on blue mold resistance, accounting for 27.5% of the experimental variability. The QTL mapped from 67.3 to 74 cM on linkage group 3 of the GMAL4593 genetic linkage map. qM-Pe10.1 mapped from 73.6 to 81.8 cM on linkage group 10. It had less of an effect on resistance, accounting for 14% of the experimental variation. 'Royal Gala' was the primary contributor to the resistance effect of this QTL. However, resistance-associated alleles in both parents appeared to contribute to the least square mean blue mold lesion diameter in an additive manner at qM-Pe10.1. A GMAL4593 genetic linkage map composed of simple sequence repeats and 'Golden Delicious' single nucleotide polymorphism markers was able to detect qM-Pe10.1, but failed to detect qM-Pe3.1. The subsequent addition of genotyping-by-sequencing markers to the linkage map provided better coverage of the PI613981 genome on linkage group 3 and facilitated discovery of qM-Pe3.1. A DNA test for qM-Pe3.1 has been developed and is currently being evaluated for its ability to predict blue mold resistance in progeny segregating for qM-Pe3.1. Due to the long juvenility of apple, the availability of a DNA test to screen for the presence of qM-Pe3.1 at the seedling stage will greatly improve efficiency of breeding apple for blue mold resistance.

MeSH terms

  • Chromosome Mapping
  • Disease Resistance / genetics*
  • Fruit / genetics
  • Fruit / immunology
  • Fruit / microbiology
  • Genetic Linkage
  • Genetic Markers
  • Genome, Plant*
  • Genotype*
  • High-Throughput Nucleotide Sequencing
  • Malus / genetics*
  • Malus / immunology
  • Malus / microbiology
  • Microsatellite Repeats
  • Penicillium / pathogenicity
  • Penicillium / physiology
  • Phenotype
  • Plant Diseases / genetics*
  • Plant Diseases / immunology
  • Plant Diseases / microbiology
  • Polymorphism, Single Nucleotide
  • Quantitative Trait Loci*
  • Quantitative Trait, Heritable

Substances

  • Genetic Markers

Grants and funding

This research was funded in large-part by Research Grant No. US-4774-14C from BARD, The United States—Israel Binational Agricultural Research and Development Fund (https://www.bard-isus.com/); and additionally by the Washington Tree Fruit Research Commission (http://www.treefruitresearch.com/) project numbers AP-08-804 and CP-10-101; and the USDA National Institute of Food and Agriculture—Specialty Crop Research Initiative (https://nifa.usda.gov/funding-opportunity/specialty-crop-research-initiative-scri) project RosBREED: Combining disease resistance with horticultural quality in new Rosaceous cultivars (2014-51181-22378). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.