title: Resistance to gray leaf spot of maize: genetic architecture and mechanisms elucidated through nested association mapping and near-isogenic line analysis.
abstract: Gray leaf spot (GLS), caused by Cercospora zeae-maydis and Cercospora zeina, is one of the most important diseases of maize worldwide. The pathogen has a necrotrophic lifestyle and no major genes are known for GLS. Quantitative resistance, although poorly understood, is important for GLS management. We used genetic mapping to refine understanding of the genetic architecture of GLS resistance and to develop hypotheses regarding the mechanisms underlying quantitative disease resistance (QDR) loci. Nested association mapping (NAM) was used to identify 16 quantitative trait loci (QTL) for QDR to GLS, including seven novel QTL, each of which demonstrated allelic series with significant effects above and below the magnitude of the B73 reference allele. Alleles at three QTL, qGLS1.04, qGLS2.09, and qGLS4.05, conferred disease reductions of greater than 10%. Interactions between loci were detected for three pairs of loci, including an interaction between iqGLS4.05 and qGLS7.03. Near-isogenic lines (NILs) were developed to confirm and fine-map three of the 16 QTL, and to develop hypotheses regarding mechanisms of resistance. qGLS1.04 was fine-mapped from an interval of 27.0 Mb to two intervals of 6.5 Mb and 5.2 Mb, consistent with the hypothesis that multiple genes underlie highly significant QTL identified by NAM. qGLS2.09, which was also associated with maturity (days to anthesis) and with resistance to southern leaf blight, was narrowed to a 4-Mb interval. The distance between major leaf veins was strongly associated with resistance to GLS at qGLS4.05. NILs for qGLS1.04 were treated with the C. zeae-maydis toxin cercosporin to test the role of host-specific toxin in QDR. Cercosporin exposure increased expression of a putative flavin-monooxygenase (FMO) gene, a candidate detoxification-related gene underlying qGLS1.04. This integrated approach to confirming QTL and characterizing the potential underlying mechanisms advances the understanding of QDR and will facilitate the development of resistant varieties.
authors.affiliation: School of Integrative Plant Sciences, Cornell University, Ithaca, New York, United States of America.
authors.forename: Jacqueline M
authors.initials: JM
authors.lastname: Benson
authors.affiliation: Department of Agronomy, Kansas State University, Manhattan, Kansas, United States of America.
authors.forename: Jesse A
authors.initials: JA
authors.lastname: Poland
authors.affiliation: 203 Solutions LLC, Baltimore, Maryland, United States of America.
authors.forename: Brent M
authors.initials: BM
authors.lastname: Benson
authors.affiliation: Department of Plant Pathology, Physiology and Weed Science, Virginia Polytechnic Institute, Blacksburg, Virginia, United States of America.
authors.forename: Erik L
authors.initials: EL
authors.lastname: Stromberg
authors.affiliation: School of Integrative Plant Sciences, Cornell University, Ithaca, New York, United States of America.
authors.forename: Rebecca J
authors.initials: RJ
authors.lastname: Nelson
mesh_terms: D001203:Ascomycota / Q000502:physiology*; D058685:Genetic Pleiotropy; D010105:Oxygenases / Q000235:genetics; D010569:Perylene / Q000031:analogs & derivatives / Q000494:pharmacology; D010935:Plant Diseases / Q000235:genetics* / Q000276:immunology*; D018515:Plant Leaves / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D040641:Quantitative Trait Loci; D003313:Zea mays / Q000145:classification / Q000235:genetics* / Q000276:immunology*
chemical_list: D010569:Perylene; C026363:cercosporin; D010105:Oxygenases; C020066:dimethylaniline monooxygenase (N-oxide forming)