The fungus Fusarium verticillioides causes Fusarium ear rot (FER) and produces the mycotoxin fumonisin in maize, reducing yields and harming human and animal health. Resistances to FER and fumonisin contamination per se are quantitatively controlled, moderately to highly heritable, and genetically correlated. Yield components and biochemical pathways involved in general plant processes have been associated with FER and fumonisin, suggesting that the genetics underlying resistance may also influence morphology and physiology (and vice versa). Here FER and fumonisin data were combined with 30 publicly available morphophysiological phenotypes from the maize core diversity panel and four recombinant inbred line families to dissect the genetics of per se and morphophysiologically mediated-resistance via correlation analyses, linkage mapping, genome-wide association, and genomic prediction and variance partitioning.
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