Submitted to: Tomato Breeders Roundtable Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 12/2/2000
Publication Date: N/A
Citation: N/A Interpretive Summary: Anthracnose is a serious fruit rot disease of tomatoes grown in regions of the northeast and midwestern U.S. and south-central Canada for processing applications. Cultural techniques including fungicide application and crop rotation provide incomplete protection from this fungal pathogen. High levels of genetic resistance to anthracnose exist in wild or unadapted tomato germplasm, but this resistance has been difficult to transfer into elite materials with an intensity equal to that observed in the wild donor parent. Difficulty in transferring the high level of resistance observed in small-fruited germplasm to commercial type lines was attributed in part to the occurrence of multiple genetic factors, each with a relatively small effect, which influence resistance. Molecular markers linked to resistance genes were identified. These markers will facilitate transfer of anthracnose resistance genes from wild germplasm into cultivated tomato. Results will be used by state, federal and private researchers to develop improved germplasm with genetic resistance to fungal pathogens in tomato.
Technical Abstract: Genetic characterization of anthracnose resistance in tomato was accomplished using populations developed from crosses between an anthracnose susceptible cultivar 'US28' and three resistant breeding lines which varied in degree of anthracnose resistance and relative stage of adaptation for commercial use. Anthracnose lesion diameters were scored in inoculated fruit of parental, F1, F2, and backcross generations within each cross. A RAPD analysis of an F2 population derived from the cross of 'US28' and the highly resistant but unadapted small fruited line, 115-4, was utilized to detect QTLs for anthracnose resistance. Heritabilities for resistance were moderate and declined as relative anthracnose susceptibility of the resistant parent increased coincident with increasing horticultural adaptation. Genetic variance for anthracnose resistance was primarily additive. The minimum number of loci conditioning anthracnose resistance declined during attempts to transfer high levels of resistance exhibited by line 115-4 into adapted breeding lines. Putative RAPD markers liked to loci which influence resistance were identified. The phenotypic variation for anthracnose resistance explained by any individual QTL was small.