Species-Specific Regulatory Complexes Shape Quan??ta??ve Resistance to a Necrotrophic Pathogen in Wild Tomatoes.
Wild relatives of crop species possess diverse levels of quantitative disease resistance (QDR) to biotic stresses, yet the genomic and regulatory mechanisms underlying these differences are not well understood. In particular, how QDR against a generalist necrotrophic pathogen evolved and whether it is driven by conserved or species-specific regulatory networks remains unclear. Here, we examined the transcriptomic responses of five diverse wild tomato species that span a gradient of QDR. we initially hypothesized that conserved regulatory modules might control QDR. Instead, Using differential gene expression analysis and weighted gene co-expression network analysis (WGCNA), we find instead that species-specific regulatory features, encompassing both infection-induced and constitutively expressed genes, predominantly shape QDR levels. Although we identified an ethylene response factor (ERF-D6) among candidate genes for QDR-regulation, it did not fully account for the phenotypic variation. To further dissect the evolutionary basis of these regulatory patterns, we performed phylotranscriptomic analyses on gene co-regulatory networks. Strikingly, QDR-associated gene sets were enriched for evolutionarily older genes, suggesting that ancient gene functions have been co-opted rather than derived from recent gene family expansions. These results provide new insights into the evolutionary and regulatory complexity governing QDR and underscore the importance of species-specific gene regulation in shaping resistance against a cosmopolitan necrotrophic pathogen. Overall design: QuantSeq 3' Sequencing (gene-expression profiling) experiment with five wild Solanum species (S. Chilense, S. Habrochaites, S. Penellii. S. Lycopersicoides, S. Pimpinellifolium) contrasting one susceptible and one more resistant genotype in Sclerotinia sclerotiorum infected and mock-conditions. Samples from detached leaves were collected relative to lesion development during the lesion expansion.