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2019 ASHS Annual Conference

Mapping QTL Associated with Anthracnose Resistance in Tomato

Wednesday, July 24, 2019
Cohiba 5-11 (Tropicana Las Vegas)
John R. Stommel, USDA, ARS, GIFVL, Beltsville, MD
Umesh Reddy, Professor, West Virginia State University, INSTITUTE, WV
Carlos Lopez Ortiz, West Virginia State University, Institute, WV
Venkata Lakshmi Abburi, West Virginia State University, Institute, WV
Padma Nimmakayala, Professor, West Virginia State University, Institute, WV
Anthracnose caused by Colletotrichum species is a serious disease of Solanaceous crops grown in North America. It is endemic in production regions of the Eastern and Midwestern United States and south-central Canada. We have selected an unadapted small-fruited tomato line, designated 95L368, that exhibits a high level of resistance to a broad range of Colletotrichum species that cause anthracnose on ripe tomato fruit. Resistance in 95L368 was primarily additive with two to three genetic factors estimated to be segregating for resistance. Utilizing a recombinant inbred line population that we developed from a cross of 95L368 and a susceptible tomato line, genotype by sequencing (GBS) was used to identify and map genomic regions associated with anthracnose lesion development. Using GBS, 15300 polymorphic SNPs were identified of which 1692 SNPs were mapped, spanning a length of 2519cM. A genetic map was constructed with a marker density of 1.48 SNP per cM. Lesion development in fruit for individual RILs was scored over two years. Our analysis resolved only three common QTLs (chromosomes 3, 6, and 9) that showed significant effects for both years. For chromosomes 6, we located six QTL peaks at the genomic region (9.6 Mb) located between 41717475 and 51338695. Percent of variance explained by these peaks ranged from 4.2 to 5.7% (LOD 3.21 to 4.34) for the first year and 5.7 to 22% (LOD 13.01 to 14.38) for the second year. On chromosome 9, we located QTL peaks in a region with genome size of 14Mb located between the position 53457523 and 67973214. Percent of variance explained by these regions varied from 4.1 to 6.2% in the first year and 5.5 to 11.2% for the second year. QTLs in other chromosomes (2, 8, 10) manifested strong QTL × year interaction, showing significant effects in the first year and no effect in the second year. Research is ongoing to identify candidate genes in these regions that are associated with lesion development.