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1.
Theor Appl Genet ; 129(6): 1217-29, 2016 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-26971113

RESUMEN

KEY MESSAGE: A major QTL ( qRtsc8 - 1 ) conditioning resistance to tar spot complex of maize and occurring at a frequency of 3.5 % across 890 maize inbred lines. Tar spot complex (TSC) is a highly destructive disease of maize found in some countries in America. Identification of TSC resistant germplasm and elucidating the genetic mechanism of resistance is crucial for the use of host resistance to manage this disease. We evaluated 890 elite maize inbred lines in multiple environments and used genome wide association analysis (GWAS) with genotypic data from Illumina MaizeSNP50 BeadChip containing 56 K SNPs to dissect the genetics of TSC resistance. GWAS results were validated through linkage analysis in three bi-parental populations derived from different resistant and susceptible parents. Through GWAS, three TSC resistance loci were identified on chromosome 2, 7 and 8 (-log10 (p) > 5.99). A major quantitative resistance locus (QTL) designated qRtsc8-1, was detected on maize chromosome bin 8.03. qRtsc8-1, was confirmed in three independent bi-parental populations and it accounted for 18-43 % of the observed phenotypic variation for TSC. A rare haplotype within the qRtsc8-1 region, occurring at a frequency of 3.5 % increased TSC resistance by 14 %. Candidate gene analysis revealed that a leucine-rich repeat receptor-like protein (LRR-RLKs) gene family maybe the candidate gene for qRtsc8-1. Identification and localization of a major locus conditioning TSC resistance provides the foundation for fine mapping qRtsc8-1 and developing functional markers for improving TSC resistance in maize breeding programs. To the best of our knowledge, this is the first report of a major QTL for TSC resistance.


Asunto(s)
Resistencia a la Enfermedad/genética , Enfermedades de las Plantas/genética , Sitios de Carácter Cuantitativo , Zea mays/genética , Ascomicetos , Mapeo Cromosómico , Estudios de Asociación Genética , Ligamiento Genético , Genotipo , Haplotipos , Fenotipo , Enfermedades de las Plantas/microbiología , Polimorfismo de Nucleótido Simple
2.
BMC Plant Biol ; 15: 206, 2015 Aug 20.
Artículo en Inglés | MEDLINE | ID: mdl-26289207

RESUMEN

BACKGROUND: Northern corn leaf blight (NCLB) caused by Exserohilum turcicum is a destructive disease in maize. Using host resistance to minimize the detrimental effects of NCLB on maize productivity is the most cost-effective and appealing disease management strategy. However, this requires the identification and use of stable resistance genes that are effective across different environments. RESULTS: We evaluated a diverse maize population comprised of 999 inbred lines across different environments for resistance to NCLB. To identify genomic regions associated with NCLB resistance in maize, a genome-wide association analysis was conducted using 56,110 single-nucleotide polymorphism markers. Single-marker and haplotype-based associations, as well as Anderson-Darling tests, identified alleles significantly associated with NCLB resistance. The single-marker and haplotype-based association mappings identified twelve and ten loci (genes), respectively, that were significantly associated with resistance to NCLB. Additionally, by dividing the population into three subgroups and performing Anderson-Darling tests, eighty one genes were detected, and twelve of them were related to plant defense. Identical defense genes were identified using the three analyses. CONCLUSION: An association panel including 999 diverse lines was evaluated for resistance to NCLB in multiple environments, and a large number of resistant lines were identified and can be used as reliable resistance resource in maize breeding program. Genome-wide association study reveals that NCLB resistance is a complex trait which is under the control of many minor genes with relatively low effects. Pyramiding these genes in the same background is likely to result in stable resistance to NCLB.


Asunto(s)
Mapeo Cromosómico , Resistencia a la Enfermedad/genética , Estudio de Asociación del Genoma Completo , Enfermedades de las Plantas/genética , Hojas de la Planta/microbiología , Zea mays/genética , Zea mays/microbiología , Análisis de Varianza , Cromosomas de las Plantas/genética , Genes de Plantas , Estudios de Asociación Genética , Sitios Genéticos , Haplotipos/genética , Patrón de Herencia/genética , Anotación de Secuencia Molecular , Fenotipo , Enfermedades de las Plantas/microbiología , Hojas de la Planta/genética , Polimorfismo de Nucleótido Simple/genética
3.
Genet. mol. biol ; 31(1): 89-97, 2008. tab
Artículo en Inglés | LILACS | ID: lil-476157

RESUMEN

Breeding programs for acid-soil tolerance are desirable as a relatively inexpensive and permanent way for increasing maize (Zea mays L.) yield on these soils. Our objective was to compare the genetic effects controlling the expression of maize traits in acid and non-acid soils. Seven related and one unrelated inbred lines, with different levels of tolerance to acid soil, and their F1, F2, BC1, and BC2 generations were evaluated in four acid and two non-acid soils. Estimates of additive, dominance, and epistatic effects were computed for grain yield, plant height, days to mid-silk, and prolificacy, using the generation means analysis procedure. For all traits the major part of the variation was accounted for by additive and dominance effects, with dominance effects being more important than additive and epistatic effects for both acid and non-acid soils. Epistatic effects were significant for some crosses only, being more pronounced for plant height than for the other traits. Furthermore, epistatic effects were randomly distributed among the crosses and were not related to the grain yield of the single-crosses (F1's) and to the genetic relationships of the inbreds in either type of soil. The results suggest that similar pooled gene effects control the expression of the traits assessed in both acid and non-acid soils.


Asunto(s)
Acidez del Suelo/análisis , Zea mays/genética , Análisis de Varianza , Variación Genética , Herencia
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