Abstract
The fungus Fusarium verticillioides can infect maize ears, causing Fusarium ear rot (FER) and contaminating the grain with fumonisins (FUM), which are harmful to humans and animals. Breeding for resistance to FER and FUM and post-harvest sorting of grain are two strategies for reducing FUM in the food system. Kernel and cob tissues have been previously associated with differential FER and FUM. Four recombinant inbred line families from the maize nested associated mapping population were grown and inoculated with F. verticillioides across four environments, and we evaluated the kernels for external and internal infection severity as well as FUM contamination. We also employed publicly available phenotypes on innate ear morphology to explore genetic relationships between ear architecture and resistance to FER and FUM. The four families revealed wide variation in external symptomatology at the phenotypic level. Kernel bulk density under inoculation was an accurate indicator of FUM levels. Genotypes with lower kernel density—under both inoculated and uninoculated conditions—and larger cobs were more susceptible to infection and FUM contamination. Quantitative trait locus (QTL) intervals could be classified as putatively resistance-specific and putatively shared for ear and resistance traits. Both types of QTL mapped in this study had substantial overlap with previously reported loci for resistance to FER and FUM. Ear morphology may be a component of resistance to F. verticillioides infection and FUM accumulation.
Highlights
In maize (Zea mays L), the fungus Fusarium verticillioides causes Fusarium ear rot (FER) and contaminates grain with fumonisins (FUM), a family of mycotoxins produced by Fusarium spp. [1]
We inoculated the ears with toothpicks coated in F. verticillioides spores, a method that has previously been shown to reveal cob and kernel resistance mechanisms [33]
Given the symptomatological variation present in the four recombinant inbred line (RIL) families, we sought to test the extent to which innate ear architecture played a role in resistance to F. verticillioides infection (FVI) using publicly available data on cob density (CobDen), diameter (CobDiam), length (CobLen), mass (CobMass), and volume (CobVol) as well as uninoculated kernel bulk density (BDENuninoc )
Summary
In maize (Zea mays L), the fungus Fusarium verticillioides causes Fusarium ear rot (FER) and contaminates grain with fumonisins (FUM), a family of mycotoxins produced by Fusarium spp. [1]. Genetic resistance to FER and FUM contamination in maize is moderately to highly heritable and quantitatively controlled, making breeding for durable resistance feasible [19,20,21,22]. Both morphological and biochemical characteristics have been shown to contribute genetic resistance. Variation in external symptomatology of kernels infected with F. verticillioides has been associated with differential FUM accumulation [33,37,38,39], suggesting that qualitative measures of kernel symptom severity are important components of resistance. Qualitative, external, and internal indicators of FVI severity as well as publicly available data on ear architecture phenotypes [41,42] to dissect the genetic mechanisms underlying FVI-specific and ear-mediated resistance to FVI and FUM accumulation in four NAM RIL families
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