Caspase inhibitors reduce symptom development and limit bacterial proliferation in susceptible plant tissues

Abstract

How plant pathogenic bacteria kill plant cells and what benefit killing presents to bacteria residing in intercellular spaces remains a topic of considerable interest in plant pathology. Activating a host cell's programmed cell death pathway may provide a means to successfully initiate and maintain an infection of a host for both animal and plant bacterial pathogens. Co-infiltration of tetrapeptide caspase inhibitors [e.g. acetyl-asp-glu-val-asp-aldehyde (Ac-DEVD-CHO)] with plant pathogenic bacteria in a susceptible plant host resulted in reduced plant cell death and a virtual cessation in bacterial growth. Reductions of 1000- to 10000-fold could be achieved when measurements were performed 3 days post-inoculation. The co-infiltration of DEVD-CHO with Pseudomonas syringae pv. tabaci into susceptible tobacco diminished the level of expression of all pathogenesis related transcripts assayed. No non-specific and deleterious impact of the caspase inhibitors on bacteria or plant cells was observed. The results of these experiments are among the first to suggest that necrotrophic, phytopathogenic bacteria are activating an apoptosis equivalent of programmed plant cell death as part of pathogenesis. Results also suggest that bacteria derive a growth-sustaining benefit from activating programmed plant cell death.