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SUMMARY: By conducting hierarchical clustering along a sliding window, we generated haplotypes across hundreds of re‐sequenced genomes in a few hours. We leveraged our method to define cryptic introgressions underlying disease resistance in tomato (Solanum lycopersicum L.) and to discover resistant germplasm in the tomato seed bank. The genomes of 9 accessions with early blight (Alternaria linariae) disease resistance were newly sequenced and analyzed together with published sequences for 770 tomato and wild species accessions, most of which are available in germplasm collections. Identification of common ancestral haplotypes among resistant germplasm enabled rapid fine mapping of recently discovered quantitative trait loci (QTL) conferring resistance and the identification of possible causal variants. The source of the early blight QTL EB‐9 was traced to a vintage tomato named 'Devon Surprise'. Another QTL, EB‐5, as well as resistance to bacterial spot disease (Xanthomonas spp.), was traced to Hawaii 7998. A genomic survey of all accessions forecasted EB‐9‐derived resistance in several heirloom tomatoes, accessions of S. lycopersicum var. cerasiforme, and S. pimpinellifolium PI 37009. Our haplotype‐based predictions were validated by screening the accessions against the causal pathogen. There was little evidence of EB‐5 prevalence in surveyed contemporary germplasm, presenting an opportunity to bolster tomato disease resistance by adding this rare locus. Our work demonstrates practical insights that can be derived from the efficient processing of large genome‐scale datasets, including rapid functional prediction of disease resistance QTL in diverse genetic backgrounds. Finally, our work finds more efficient ways to leverage public genetic resources for crop improvement. Significance Statement: We introduce a powerful windowed haplotype classification method that can efficiently detect local homology across genomes and predict biological traits in germplasm. We co‐analyzed hundreds of genomic sequences to define and predict introgressions conferring resistance to early blight disease of tomato. These predictions were validated in planta with pathology experiments, demonstrating the functional prediction of quantitative resistance of breeding and research significance. Our haplotype clustering and prediction method is broadly applicable to crops with large genomic datasets. [ABSTRACT FROM AUTHOR]

We used molecular markers to identify quantitative trait loci (QTL) that confer resistance in the field to Xanthomonas campestris pv. vesicatoria race T1, a causal agent of bacterial spot of tomato. An F2 population derived from a cross between Hawaii 7998 (H 7998) and an elite breeding line, Ohio 88119, was used for the initial identification of an association between molecular markers and resistance as measured by bacterial populations in individual plants in the greenhouse. Polymorphism in this cross between a Lycopersicon esculentum donor of resistance and an elite L. esculentum parent was limited. The targeted use of a core set of 148 polymerase chain reaction-based markers that were identified as polymorphic in L. esculentum × L. esculentum crosses resulted in the identification of 37 markers that were polymorphic for the cross of interest. Previous studies using an H 7998 × L. pennellii wide cross implicated three loci, Rx1, Rx2, and Rx3, in the hypersensitive response to T1 strains. Markers that we identified were linked to the Rx1 and Rx3 loci, but no markers were identified in the region of chromosome 1 where Rx2 islocated. Single marker-trait analysis suggested that chromosome 5, near the Rx3 locus, contributed to reduced bacterial populations in lines carrylng the locus from H 7998. The locus on chromosome 5 explained 25% of the phenotypic variation in bacterial populations developing in infected plants. An advanced backcross population and subsequent inbred backcross lines developed using Ohio 88119 as a recurrent parent were used to confirm QTL associations detected in the F2 population. Markers on chromosome 5 explained 41% of the phenotypic variation for resistance in replicated field trials. In contrast, the Rx1 locus on chromosome I did not play a role in resistance to X. campestris pv. vesicatoria race T1 strains as measured by bacterial populations in the greenhouse or symptoms in the field. A locus from H 7998 on chromosome 4 was associated with susceptibility to disease and explained 11% of the total phenotypic variation. Additional variation in resistance was explained by plant maturity (6%), with early maturing families expressing lower levels of resistance, and plant habit (6%), with indeterminate plants displaying more resistance. The markers linked to Rx3 will be useful in selection for resistance in elite x elite crosses. [ABSTRACT FROM AUTHOR]

Bacterial spot of tomato is a foliar disease caused by four Xanthomonas species. Identifying genetic resistance in wild tomatoes and subsequent breeding of varieties has been a strategy to reduce the loss from this disease because control using pesticides has been ineffective. Three independent sources of resistance have been identified with quantitative trait loci (QTL) mapping to the centromeric region on chromosome 11. These sources are derived from Hawaii 7998 (QTL-11A), PI 114490 (QTL-11B), and LA2533 (QTL-11C). To determine which QTL introgression from chromosome 11 provides the greatest resistance to multiple species, we developed near-isogenic lines (NILs) using marker-assisted backcrossing. In parallel, we developed an NIL that contains Rx-4/Xv3 , which provides major gene resistance to Xanthomonas perforans . Additionally, we combined Rx-4/Xv3 resistance with QTL-11A. These sources of resistance were independently introduced into the susceptible parent, OH88119. During a 3-year period from 2016 to 2018, we evaluated backcross-derived families and NILs from each source in independent field trials inoculated with X. perforans , X. euvesicatoria , or X. gardneri . Our results suggest that both QTL-11C and QTL-11A combined with Rx-4/Xv3 provide effective genetic resistance against multiple Xanthomonas species. In addition, we provide evidence for additive to dominant genetic action for the QTL introgressions.