P-020 - Co-optation of Transcription Factors Drives Evolution of Quantitative Disease Resistance Against a Necrotrophic Pathogen.

Wild crop relatives exhibit diverse levels of quantitative disease resistance (QDR), but the underlying genomic and regulatory factors remain unclear. In particular, whether QDR against generalist necrotrophic pathogens evolved via conserved or species-specific regulatory networks is unknown. Here, we examined the transcriptomic responses of five diverse wild tomato (Solanum) species spanning a QDR gradient using differential gene expression analysis and weighted gene co-expression network analysis (WGCNA). We find that species-specific regulatory features, encompassing infection-induced and constitutively expressed genes, predominantly shape QDR levels. To further dissect the evolutionary dynamics of these regulatory patterns, we performed phylotranscriptomic analyses on gene regulatory networks. We show that the conserved NAC29 transcription factor co-opted a role in QDR in Solanum pennellii. Although NAC29 is conserved across all five species, only in S. pennellii is it induced upon infection and associated with novel defence-related "executor" genes. This finding highlights the species-specific rewiring of gene regulatory networks by repurposing a conserved regulatory element to enhance resistance against pathogens. These results offer new insights into the evolutionary and regulatory complexity underlying QDR and emphasise the significance of species-specific gene regulation in shaping resistance against generalist necrotrophic pathogens.