| Summary: | Tomato (<i>Solanum lycopersicum</i> L.) is one of the most widely grown vegetables in the world and is impacted by many diseases which cause yield reduction or even crop failure. Breeding for disease resistance is thus a key objective in tomato improvement. Since disease arises from a compatible interaction between a plant and a pathogen, a mutation which alters a plant susceptibility (S) gene facilitating compatibility may induce broad-spectrum and durable plant resistance. Here, we report on a genome-wide analysis of a set of 360 tomato genotypes, with the goal of identifying defective S-gene alleles as a potential source for the breeding of resistance. A set of 125 gene homologs of 10 S-genes (<i>PMR 4</i>, <i>PMR5</i>, <i>PMR6</i>, <i>MLO</i>, <i>BIK1</i>, <i>DMR1</i>, <i>DMR6</i>, <i>DND1</i>, <i>CPR5</i>, and <i>SR1</i>) were analyzed. Their genomic sequences were examined and SNPs/indels were annotated using the SNPeff pipeline. A total of 54,000 SNPs/indels were identified, among which 1300 were estimated to have a moderate impact (non-synonymous variants), while 120 were estimated to have a high impact (e.g., missense/nonsense/frameshift variants). The latter were then analyzed for their effect on gene functionality. A total of 103 genotypes showed one high-impact mutation in at least one of the scouted genes, while in 10 genotypes, more than 4 high-impact mutations in as many genes were detected. A set of 10 SNPs were validated through Sanger sequencing. Three genotypes carrying high-impact homozygous SNPs in S-genes were infected with <i>Oidium neolycopersici</i>, and two highlighted a significantly reduced susceptibility to the fungus. The existing mutations fall within the scope of a history of safe use and can be useful to guide risk assessment in evaluating the effect of new genomic techniques.
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