Submitted to: Aflatoxin Elimination Workshop Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 11/16/2005
Publication Date: 11/30/2005
Citation: Holland, J.B. 2005. Genetics and breeding of host resistance to fusarium ear rot and fumonisin contamination. Aflatoxin Elimination Workshop Proceedings. Interpretive Summary:
Technical Abstract: To investigate the inheritance of resistance to Fusarium ear rot and fumonisin contamination in maize, we estimated heritabilities and genetic correlations of these two aspects of disease in two maize populations. One population of 215 BC1S1 lines derived from the first backcross of GE440 to FR1064 (GEFR population) was developed by Dr. Don White), and was tested in replicated, double-inoculated field trials in four environments. The second population was 143 recombinant inbred lines derived from the cross of NC300 to B104 (NCB population), developed by Dr. Goodman, and evaluated in three environments. Heritabilities of ear rot and fumonisin content in the GEFR population were 0.75 and 0.47, respectively, and their genetic correlation was 0.96. In the NCB population, ear rot and fumonisin content heritabilities were 0.86 and 0.80, respectively, and their genetic correlation was 0.87. These results suggest that direct selection for reduced fumonisin content is theoretically optimal for reducing susceptibility to fumonisin content, but that indirect selection against ear rot may be economically most efficient at reducing fumonisin content because ear rot is much easier and faster to score than fumonisin content. Both populations were also fingerprinted with at least 105 SSR markers. QTL for both traits were mapped in both populations, and many QTL for fumonisin were also detected in the same regions as QTL for ear rot. However, some QTL appeared to have effects on ear rot but not fumonisin, and vice versa. Therefore, indirect selection on ear rot may not be effective at selecting for all of the fumonisin-reducing alleles. QTL had relatively small effects (maximum of 18% of phenotypic variation) and were largely different between populations, so marker-assisted selection will be hindered by the genetic complexity of resistance to both traits.