The inbreds PaIa453 ae du wx and PaIa5125 ae du wx were observed to differ in field reaction to Colletotrichum graminocolum (Ces) G. N. Nils., which causes anthracnose. PaIa5125 ae du wx appeared to have less disease. No clearly defined susceptible-resistant reaction was observed in either inbred. Therefore, resistance was defined as the relative production of lesions from a given concentration of inoculum. The objectives of this research were: 1) to determine if resistance could be distinguished on a basis of lesion production, and if so, 2) to determine the genetic basis of this resistance.
Experiments were conducted in the greenhouse and the field using both inbreds, the F1 hybrid and 4 segregating populations. Inoculum was prepared from 8 isolates of C. graminocolum grown on PDA for 10 days. A standard inoculum concentration of 4.0 x 105 spores/ml was applied with a pressurized sprayer. The number of lesions was recorded on the 5th leaf of each plant in the greenhouse 10 days after inoculation. In the field, the number of lesions on the 6th leaf was recorded 10 days after inoculation. Results are presented in Tables 1 and 2.
Tables 1 and 2.
It appears that resistance determined on the basis of lesion production is present in the material tested (Tables 1, 2). A lower number of lesions was produced on PaIa5125 ae du wx when compared to PaIa453 ae du wx in both greenhouse and field inoculations. The F1 responds similarly to PaIa5125 ae du wx in the field but appears intermediate in greenhouse inoculations. This may be due to fewer replications used in the greenhouse. Heritabilities were calculated for the segregating populations using the variance associated with PaIa5125 ae du wx as an estimate of environmental variance (Table 3).
Much of the variation in these traits appears to be of genetic origin. Based on these data this resistance may be controlled by as few as one gene. From the field data, a quantitative phenotypic response and genotype may be assigned to each inbred as follows:
PaIa453 ae du wx - A1A1; 139.7 lesions; 20.7 lesions/dm2
PaIa5125 ae du wx - A2A2; 42.7 lesions; 6.9 lesions/dm2
From this the mean number of lesions and mean number of lesions per dm2 can be calculated for the segregating populations based on the proportion of genotypes present and assuming dominance:
Other genes may influence lesion number in a quantitative manner of which only one was discernible in the material used in this study. It should be emphasized that plants exhibiting resistance as described here still sustain disease, but the reduction in inoculum efficiency compounded over several cycles of disease may be effective in preventing losses.
L. V. Gregory, L. J. Seybert, J. E. Ayers and D. L. Garwood
Return to the MNL 52 On-Line Index
Return to the Maize Newsletter Index
Return to the Maize Genome Database Page