Diverse mechanisms of resistance to Fusarium verticillioides infection and fumonisin contamination in four maize recombinant inbred line families

Authors: MORALES, LAURA - Cornell University; ZILA, CHARLES - North Carolina State University; MORETA MEJIA, DANILO - Cornell University; MONTOYA ARBELAEZ, MELISSA - Cornell University; Balint-Kurti, Peter; Holland, Jim - Jim; NELSON, REBECCA - Cornell University

Submitted to: Toxins
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/1/2019
Publication Date: 3/1/2019
Citation: Morales, L., Zila, C.T., Moreta Mejia, D.E., Montoya Arbelaez, M., Balint Kurti, P.J., Holland, J.B., Nelson, R.J. 2019. Diverse mechanisms of resistance to Fusarium verticillioides infection and fumonisin contamination in four maize recombinant inbred line families. Toxins. 11:86.

Interpretive Summary: The fungus Fusarium verticillioides can infect maize ears, causing Fusarium ear rot and contaminating the grain with fumonisins which are harmful to humans and animals. Breeding for resistance and post-harvest sorting of grain are two strategies for reducing fumonisins in the food system. We have identified genetic loci associated with resistance and have shown the kernel density is strongly related to levels of resistance, providing a relatively simple way to assess resistance to Fusarium verticilliodes.

Technical 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. 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.