TitleMeta-QTL for resistance to white mold in common bean.
Publication TypeJournal Article
Year of Publication2017
AuthorsVasconcellos, RCC, O Oraguzie, B, Soler, A, Arkwazee, H, Myers, JR, Ferreira, JJ, Song, Q, McClean, P, Miklas, PN
JournalPLoS One
Volume12
Issue2
Paginatione0171685
Date Published2017
ISSN1932-6203
KeywordsAscomycota, Chromosome Mapping, Chromosomes, Plant, Disease Resistance, Genetic Linkage, Genotype, Peroxidase, Phaseolus, Plant Diseases, Plant Proteins, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Transcription Factors
Abstract

White mold, caused by the fungus Sclerotinia sclerotiorum (Lib.) de Bary, is a major disease that limits common bean production and quality worldwide. The host-pathogen interaction is complex, with partial resistance in the host inherited as a quantitative trait with low to moderate heritability. Our objective was to identify meta-QTL conditioning partial resistance to white mold from individual QTL identified across multiple populations and environments. The physical positions for 37 individual QTL were identified across 14 recombinant inbred bi-parental populations (six new, three re-genotyped, and five from the literature). A meta-QTL analysis of the 37 QTL was conducted using the genetic linkage map of Stampede x Red Hawk population as the reference. The 37 QTL condensed into 17 named loci (12 previously named and five new) of which nine were defined as meta-QTL WM1.1, WM2.2, WM3.1, WM5.4, WM6.2, WM7.1, WM7.4, WM7.5, and WM8.3. The nine meta-QTL had confidence intervals ranging from 0.65 to 9.41 Mb. Candidate genes shown to express under S. sclerotiorum infection in other studies, including cell wall receptor kinase, COI1, ethylene responsive transcription factor, peroxidase, and MYB transcription factor, were found within the confidence interval for five of the meta-QTL. The nine meta-QTL are recommended as potential targets for MAS for partial resistance to white mold in common bean.

DOI10.1371/journal.pone.0171685
Alternate JournalPLoS ONE
PubMed ID28199342
PubMed Central IDPMC5310892