|Munkvold, Gary - IOWA ST UNIV, AMES, IA|
Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 11, 2002
Publication Date: November 20, 2002
Citation: Desjardins, A.E., Munkvold, G.P., Plattner, R.D., Proctor, R. 2002. Fum1-a gene required for fumonisin biosynthesis but not for maize ear rot and ear infection by gibberella moniliformis in field tests. Molecular Plant-Microbe Interactions. 15(11): 1157-1164. Interpretive Summary: Fusarium verticillioides is a fungus that causes corn ear rot and contaminates corn grain with harmful fumonisin toxins. In this study we used genetic engineering to produce fumonisin knock-out mutants of this fungus. We then showed that fumonisin knock-out mutants were able to infect corn ears, but produced no fumonisins in the grain. This study showed that fumonisins are not required for this fungus to infect corn plants and to cause ear rot. This study indicates that we may be able to prevent fumonisin contamination of corn grain by using fumonisin nonproducing strains of this fungus to compete with the fumonisin producing strains that are present naturally in corn fields. Farmers and consumers will benefit if we can reduce fumonisin contamination of corn.
Technical Abstract: Fumonisin-nonproducing mutants were obtained by disrupting FUM1 (previously FUM5), the gene encoding a polyketide synthase required for fumonisin biosynthesis. Maize ear rot, ear infection, and fumonisin contamination were assessed by silk-channel injection in 1999 and 2000, and also by spray application onto maize silks, injection into maize stalks, and application with maize seeds at planting in 1999. Ear rot was evaluated by visual assessment of whole ears and by calculating percentage of symptomatic kernels by weight. Fumonisin levels in kernels were determined by high-performance liquid chromatography. The presence of applied strains in kernels was determined by analysis of recovered isolates for genetic markers and fumonisin production. Two independent fumonisin-nonproducing (fum1-3 and fum1-4) mutants were similar to their respective fumonisin-producing (FUM1-1) progenitor strains in ability to cause ear rot following silk-channel injection, and also were similar in ability to infect maize ears following application by all four methods tested. This evidence confirms that fumonisins are not required for G. moniliformis to cause maize ear rot and ear infection.