Submitted to: Journal of American Society of Horticulture Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/8/1997
Publication Date: N/A
Citation: N/A Interpretive Summary: Tomato anthracnose is a disease which primarily affects ripe tomato fruit. Infected fruit have a very short vine or shelf life and are susceptible to secondary infections. Transfer of appreciable levels of genetic resistance from wild relatives of tomato to breeding lines and elite commercial materials has proven difficult. This may be attributed to the loss of multiple genetic factors during cultivar development which influence anthracnose resistance. Inheritance of resistance to tomato anthracnose was evaluated in populations from crosses between adapted resistant and susceptible tomato lines. Data analysis revealed that cumulative effects of a number of genes and interactions between these genes are important in anthracnose resistance. A moderate heritability estimate suggests that resistance can be measured with reasonable accuracy. Estimation of the number of genetic factors segregating for anthracnose resistance suggested the presence of one gene or, more likely, group of genes which influence anthracnose resistance. This research will benefit geneticists and breeders in developing disease resistant tomato cultivars and will reduce pesticide usage and contribute to a safer, more profitable production environment.
Technical Abstract: Inheritance of resistance to tomato anthracnose caused by Colletotrichum coccodes (Wallr.) S.J. Hughes was evaluated in parental, F1, F2, and backcross populations developed from crosses between adapted resistant (88B147) and susceptible (90L24) tomato (Lycopersicon esculentum Mill.) breeding lines. Resistance was evaluated via measurement of lesion diameters in puncture inoculated ripe fruit of field grown plants. Backcross and F2 populations exhibited continuous distributions suggesting multigenic control of anthracnose resistance. Anthracnose resistance was partially dominant to susceptibility. Using generation means analysis, gene action in these populations was best explained by an additive- dominance model with additive x additive epistatic effects. A broad sense heritability (H) of 0.42 was estimated for resistance to C. coccodes. One gene or linkage group was estimated to control segregation for anthracnose resistance in the cross of 90L24 x 88B147.