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Analysis of Resistance to Fusarium Wilt Race 3 in Accessions of the Wild Tomato Species Solanum pennellii

Thursday, August 6, 2015: 10:30 AM
Oak Alley (Sheraton Hotel New Orleans)
Jian Li , University of Florida, Wimauma, FL
Samuel F. Hutton , University of Florida, Gainesville, FL
Gary E. Vallad , University of Florida, Wimauma, FL
Jeffrey B. Jones , University of Florida, Gainesville, FL
Fusarium wilt of tomato (Solanum lycopersicum), caused by the soil-borne fungal pathogen Fusarium oxysporum f. sp. lycopersici (Fol), is a common tomato disease in most tomato production regions worldwide. Developing tomato cultivars resistant to fusarium wilt has been an effective means of controlling Fol. A dominant resistance gene (I-3) to Fol race 3 was identified from the wild tomato species Solanum pennellii accession LA716, and the I-3 gene has been fine-mapped on chromosome 7. Though tomato cultivars with I-3 have been commercially available since the early 1990s, they have some undesirable traits associated with I-3, such as a higher susceptibility to bacterial spot disease and weaker vines. We have initiated a search for alternative sources of Fol race 3 resistance that might not be associated with these negative traits. Furthermore, such resistance sources may prove effective against new races of Fol that could emerge in the future. We evaluated 42 S. pennellii accessions for resistance to Fol race 3, and nearly all accessions were highly resistant. Interspecific hybrids from crosses between each accession and the Fol race 3 susceptible ‘Suncoast’ were also evaluated, and most were resistant to Fol race 3 but less so than the accessions. The F1s were backcrossed to ‘Suncoast’ to produce F1BC1 progeny, and each of these was evaluated for resistance to race 3. We used molecular markers tightly linked with I-3 to determine if this gene played a role in the resistance of each accession. Genetic analysis indicated that resistance is conferred by the I-3 locus in approximately half of the accessions tested. Analysis also determined that one or more alternative loci are also effecting resistance alone or in combination with I-3.
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