Comparing and contrasting two plant pathogens provide a unique window into the differences in the innate immune responses between dicots and monocots

The eukaryotic parasitic plant Striga asiatica and the prokaryotic Agrobacterium tumefaciens are both plant pathogens that cue on host-derived phenylpropanoids for host recognition. The onset of virulence in both pathogens is regulated by a wounding event, but one manifested in slightly different ways. S. asiatica mimics a partial wounding response by producing reactive oxygen species on host contact, whereas A. tumefaciens depends on the wounding response of host plants to generate susceptible plant cells for transformation. Despite the similarity in their chemical strategy for host recognition, A. tumefaciens and S. asiatica pathogenize non-overlapping host ranges; monocotyledonous grasses are resistant to A. tumefaciens, but susceptible to S. asiatica. These two plant pathogens then provide a unique window into the differences in the innate immunity of dicots and monocots. The engineering potential of A. tumefaciens further provides an opportunity to map the signaling landscape at the host-pathogen interface. This study represents the first example of mapping systemically the virulence inducing signal landscape in vivo and in real time. I quantified not only the concentration of wound-induced phenol and sugar signals separately, but the duration of exudation. These results demonstrated that the fundamental difference in the wounding response between dicots and grasses is communicated via their wound-induced phenol exudation. A. tumefaciens recognizes dicots by the high level and extended exudation of wound-induced phenols, whereas grasses remain invisible to A. tumefaciens by not inducing phenol exudation. The modular nature of the subterranean development of S. asiatica further provides a valuable opportunity to study genetic regulation of development via differential expression libraries. The immune response genes and phenylpropanoid biosynthetic genes found in the differential libraries highlighted again the critical roles that the wounding response and phenol production play in plant pathogenesis. Our study on the phenylpropanoid biosynthetic genes further indicated that phenolpropanoids play a most critical role in regulating plant development beyond lignin biosynthesis. Lastly, the interaction between quinolic haustorial inducers and auxin/cytokinin signaling pathways suggest a possible evolutionary route for the parasitic plants in Scrophulariaceae and Orobanchaceae to have emerged.