Efflux Pump Gene Expression in Erwinia Chrysanthemi is Induced by Exposure to Phenolic Acids

Authors: RAMANI, S - TEXAS TECH UNIVERSITY; BARABOTE, R - UC SAN DIEGO; WHEELER, D - TEXAS TECH UNIVERSITY; REVERCHON, S - NATION INST APPLIED SCIEN; TATUM, O - TEXAS TECH UNIVERSITY; MALOUF, J - UC SAN DIEGO; LUI, H - UC SAN DIEGO; PRITCHARD, L - SCOTTISH CROP RESEARCH IN; HEDLEY, P - SCOTTISH CROP RESEARCH IN; BIRCH, P - SCOTTISH CROP RESEARCH IN; TOTH, I - SCOTTISH CROP RESEARCH IN; Payton, Paxton; SAN FRANCISCO, M - TEXAS TECH UNIVERSITY

Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/20/2006
Publication Date: 3/1/2007
Citation: Ramani, S.R., Barabote, R.D., Wheeler, D.H., Reverchon, S., Tatum, O., Malouf, J., Lui, H., Pritchard, L., Hedley, P.E., Birch, P.R., Toth, I.K., Payton, P.R., San Francisco, M.J. 2007. Efflux pump gene expression in Erwinia Chrysanthemi is induced by exposure to phenolic acids. Molecular Plant-Microbe Interactions. 20(3):313-320.

Interpretive Summary: Drug efflux pumps in bacteria are recognized as major contributors to bacterial survival. In both animal and plant pathogens, efflux pump activity has been shown to be a critical part of sensitizing bacterial anti-biotic resistance, as well as the pathogenicity of the bacteria. Erwinia chrysanthemi is a common plant pathogen the causes blight or soft-rot diseases due to tissue maceration resulting from plant cell wall degradation. E. chrysamthemi is common in many vegetable, bulb, and ornamental crops. Although our understanding of E. chrysanthemi virulence factors and their regulation has become increasingly clear over the past 10 years, we have a less complete understanding of how this bacterium survives in the plant following infection and how it tolerates the onslaught of plant antimicrobial chemicals. In response to microbial attack, plants activate defense responses that lead to induction of a broad spectrum of anti-microbial defenses. These induced defenses are expressed not just locally but also in parts distant from the site of primary infection, thereby protecting the plant from spread of an infection and future attack. One of the earliest responses of plants to pathogen attack is the generation of an oxidative burst that can trigger hypersensitive cell death. This hypersensitive response (HR) is associated with increased synthesis of lignin and callose to fortify the cell from invasion by the pathogen. Subsequently, induced resistance is regulated by a network of interconnecting signal transduction pathways in which salicylic acid (SA) is a key signaling molecule. The accumulation of SA functions to amplify the host plant’s defense system and results in the induction of pathogenesis-related proteins and anti-microbial chemicals. Successful microbial pathogens utilize a variety of mechanisms to rid themselves of toxic anti-microbial compounds. Important among these mechanisms are multidrug-resistance pumps that bring about the active efflux of toxic compounds from microbial cells. Here, we show that a combination SA and its precursors, t-cinnamic acid and benzoic acid, can activate expression of specific multidrug efflux pump-encoding genes in the E. chrysanthemi and enhance survival of the bacterium in the presence of model as well as plant-derived anti-microbial chemicals. This ability of plant-pathogenic bacteria to co-opt plant defense-signaling molecules to activate multi-drug efflux pumps may have evolved to ensure bacterial survival in susceptible host plants. Studies on specific interactions between plant-derived phenolic acids and regulatory proteins in E. chrysanthemi currently are underway to allow us to more fully understand the complex signaling that occurs between pathogen and host.

Technical Abstract: Salicylic acid (SA) is an important signaling molecule in local and systemic plant resistance. Following infection by microbial pathogens and the initial oxidative burst in plants, SA accumulation functions in the amplification of defense gene expression. Production of pathogenesisrelated proteins and toxic antimicrobial chemicals serves to protect the plant from infection. Successful microbial pathogens utilize a variety of mechanisms to rid themselves of toxic antimicrobial compounds. Important among these mechanisms are multidrug-resistance pumps that bring about the active efflux of toxic compounds from microbial cells. Here, we show that a combination SA and its precursors, t-cinnamic acid and benzoic acid, can activate expression of specific multidrug efflux pump-encoding genes in the plant pathogen Erwinia chrysanthemi and enhance survival of the bacterium in the presence of model as well as plant-derived antimicrobial chemicals. This ability of plant-pathogenic bacteria to co-opt plant defense-signaling molecules to activate multidrug efflux pumps may have evolved to ensure bacterial survival in susceptible host plants.