Background: Resistance to Fusarium ear rot of maize is a quantitative and complex trait. Marker-trait associations to date have had small additive effects and were inconsistent between previous studies, likely due to the combined effects of genetic heterogeneity and low power of detection of many small effect variants. The complexity of inheritance of resistance hinders the use marker-assisted selection for ear rot resistance.
Results: We conducted a genome-wide association study (GWAS) for Fusarium ear rot resistance in a panel of 1687 diverse inbred lines from the USDA maize gene bank with 200,978 SNPs while controlling for background genetic relationships with a mixed model and identified seven single nucleotide polymorphisms (SNPs) in six genes associated with disease resistance in either the complete inbred panel (1687 lines with highly unbalanced phenotype data) or in a filtered inbred panel (734 lines with balanced phenotype data). Different sets of SNPs were detected as associated in the two different data sets. The alleles conferring greater disease resistance at all seven SNPs were rare overall (below 16%) and always higher in allele frequency in tropical maize than in temperate dent maize. Resampling analysis of the complete data set identified one robust SNP association detected as significant at a stringent p-value in 94% of data sets, each representing a random sample of 80% of the lines. All associated SNPs were in exons, but none of the genes had predicted functions with an obvious relationship to resistance to fungal infection.
Conclusions: GWAS in a very diverse maize collection identified seven SNP variants each associated with between 1% and 3% of trait variation. Because of their small effects, the value of selection on these SNPs for improving resistance to Fusarium ear rot is limited. Selection to combine these resistance alleles combined with genomic selection to improve the polygenic background resistance might be fruitful. The genes associated with resistance provide candidate gene targets for further study of the biological pathways involved in this complex disease resistance.