|Holland, Jim - Jim|
Submitted to: Aflatoxin Elimination Workshop Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 11/1/2002
Publication Date: 11/1/2002
Citation: ROBERTSON, L.A., PAYNE, G.A., WHITE, D.G., HOLLAND, J.B. MAIZE MAPPING POPULATIONS FOR IDENTIFYING QTLS FOR FUMONSIN ACCUMULATION AND EAR ROT RESISTANCE.. AFLATOXIN ELIMINATION WORKSHOP PROCEEDINGS. 2002. Interpretive Summary: The fungus Fusarium causes ear rots and associated yield losses in field corn. In addition, the fungus produces a toxin called fumonisin that is associated with diseases in animals and humans that have eaten infected corn. Little is known about the inheritance of resistance to the ear rot and fumonisin accumulation caused by the fungus. We created two corn populations from crosses between inbred lines that appear to have some resistance to the fungus to lines that are more susceptible. By studying the progeny of these crosses to determine which molecular markers tend to be co-inherited with resistance, we expect to identify the chromosomal regions that carry resistance genes.
Technical Abstract: GE440 and NC300 were identified in previous studies as potential sources for resistance to fumonisin accumulation and Fusarium ear and kernel rot. Two mapping populations, GE440 x FR1064 and NC300 x B104, were created to identify the loci associated with disease resistance and resistance to fumonisin accumulation. Our research is focused on answering two key questions: (1) Do some QTLs for ear rot resistance also confer resistance to fumonisin accumulation?, and (2) Are QTLs consistent across populations? In 2002, the GE440 x FR1064 population was grown at Mt. Olive, NC and the NC300 x B104 population was grown at Clayton, NC. Populations were replicated twice at each location. Primary ears were inoculated with a mixture of three isolates each of F. verticillioides and F. proliferatum. Inoculated ears were rated for the percentage of kernels rotted. Replicate plots of parental lines and the five most and five least rotted lines from the GE440 x FR1064 population were selected for toxin analysis. The grain was ground, bulked by plot, and evaluated for fumonisin concentration using HPLC. Our results to date indicate that QTLs for both traits are segregating in both populations. GE440 and FR1064 differed significantly for ear rot, but not for fumonisin concentration. NC300 and B104 did not differ significantly for ear rot, but NC300 did have significantly less fumonisin. Our results indicate that genes controlling Fusarium ear rot and fumonisin accumulation resistance are segregating in both populations. Therefore, we expect to be able to map QTLs for resistance to both the disease and mycotoxin accumulation in these populations.