Mapping of novel non-race 1 Verticillium wilt resistance QTLs in tomato using high-density linkage map construction

• Verticillium wilt, caused by V. dahliae , is a major threat to tomato production worldwide. • SNP markers derived from LC-WGS produced a high-density genetic linkage map. • Nine QTLs conferring resistance to non-race 1 V . dahliae in tomatoes were mapped. • Neighboring QTLs on chromosomes 4 and 5 might be the same or loosely linked loci. • QTLs on chromosomes 4 and 5 seem stable in different environments. Verticillium wilt (VW), caused by the soil-borne fungal pathogen ( Verticillium dahliae ), poses a major threat to tomato production in temperate climates, including Western North Carolina and the nearby states. There is a dire need to develop disease-resistant lines by understanding the in-depth genetic basis of unexplored VW resistance in tomato germplasms. In this study, we developed segregating genetic mapping populations (F 2 and F 3 ) derived from a cross between two tomato lines, with moderate resistance to non-race 1 isolates of V. dahliae . The statistical analysis of the disease incidence and severity across three different environments with a history of natural disease pressure showed a complex and polygenetic nature of the resistance in the germplasm affected by the environment. A high percentage of the progenies showed high VW resistance due to transgressive segregation in the mapping populations. Low-coverage whole-genome sequencing of 95 F 2 individuals was used to generate a high-density SNP database validated by the high-coverage whole-genome sequencing of the parental lines. The bioinformatics analysis revealed a total of 3269 high-quality SNP markers that were used for genetic linkage map construction spanning a total of 5516 cM in length and with an average spacing of 1.69 cM, and a moderate number of recombination events and high genomic collinearity. Multiple QTL mapping-based analyses identified 9 QTLs across five different chromosomes (2, 4, 5, 6, and 11), explaining a range of 4.40–13.36 % of the variation in VW disease severity. Three QTLs on chromosomes 4, 5, and 6 showed major effects; furthermore, two neighboring QTLs on chromosomes 4 and 5 derived from one of the parental lines are probably the same or loosely linked loci stable across the environments. The identified QTL-SNP markers also illustrated allele-specific contributions to the low disease severity index values across three different environments.