Host-pathogen interactions are shaped by a mutual flow of information that leads to responses and counter-responses in both organisms and shapes the final outcome. These studies typically focus on specialist interactions often involving NBS-LRRs. This limits any study to how singular hosts and pathogens interact largely preventing an evolutionary analysis of how the information flow may change between and within plant species. To ask questions about how plant evolution shapes the flow of information in host-pathogen interactions, we are using the generalist pathogen, Botrytis cinerea, that can successfully infect nearly every plant. Specifically, we are in the process of infecting 96 isolates on 16 different asterid and rosid plant species to conduct co-transcriptomics to understand how the system is evolving. To test the potential of the co-transcriptomics approach and to query how within species genetic variation manipulates the system, we infected 96 Botrytis isolates on Arabidopsis thaliana wild-type and mutants missing the key defense pathways, JA/coi1 and SA/npr1. This showed that there was an extensive level of communication between the two transcriptomes with the Botrytis actually being the dominant driver of the transcriptomics responses. Specifically, it was possible to measure heritability of the defense response due to the host, the pathogen and the interaction of the two (cross-species epistasis?). In combination with the pathogens genomic sequence, we were able to conduct eQTL mapping and show how genetic variation in the pathogen is connected to transcriptional variation in the host. Extending this analysis to other dicots including Tomato, Lettuce, Chicory, Sunflower, Soybean and Brassica shows that Botrytis cinerea also displays a polygenic genomic architecture in virulence on these diverse hosts. Intriguingly there was minimal effect of domestication on the host/pathogen interaction with most plant hosts showing increased resistance in the domesticated germplasm and a similar range of variation. Further, the dominant driver of the system on the plant side was species level variation with little to no signal from family or genera. This indicates that there may be little deep conservation in the specifics of how defense signaling is happening and that most of the important aspects are species specific. Using this virulence data, we were able to identify pathogen loci that control virulence across wild and domestic germplasm and these loci seem to focus on cell wall degradation, toxin production and detoxification with no identifiable MAMP/PAMP involved gene such as chitin, NEPs or mannitol. This shows that using a common generalist pathogen is allowing us to visualize how plant defense signaling is evolving across the dicots.