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ARS Home » Northeast Area » Ithaca, New York » Robert W. Holley Center for Agriculture & Health » Emerging Pests and Pathogens Research » Research » Publications at this Location » Publication #332039

Title: Comparative genomics of pseudomonas syringae pathovar tomato reveals novel chemotaxis pathways associated with motility and plant pathogenicity

item CLARKE, CHRISTOPHER - Virginia Tech
item HAYES, BYRON - Virginia Tech
item RUNDE, BRENDAN - Virginia Tech
item Markel, Eric
item WEBB, BENJAMIN - Virginia Tech
item SCHARF, BIRGIT - Virginia Tech
item Swingle, Bryan
item VINATZER, BORIS - Virginia Tech

Submitted to: PeerJ
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/15/2016
Publication Date: 10/25/2016
Citation: Clarke, C.R., Hayes, B.W., Runde, B.J., Markel, E.J., Webb, B.A., Scharf, B.E., Swingle, B.M., Vinatzer, B.A. 2016. Comparative genomics of pseudomonas syringae pathovar tomato reveals novel chemotaxis pathways associated with motility and plant pathogenicity. PeerJ. 4:e2570.

Interpretive Summary: Plant diseases occur when pathogenic organisms, like bacteria, enter and grow inside leaves and other parts of plants. Some bacteria can sense and move towards wounds and natural openings in leaves where they enter into the plant and begin the infection process. Bacteria cannot cause disease without entering the plant, which means that chemicals that block or confuse the bacterium’s sense of direction could be used to prevent disease. To achieve the goal of finding such a chemical, scientists or engineers need to know which systems to inactivate. In this study we found two gene clusters that were candidates for controlling directed movement. These genes were found in a plant pathogenic bacteria, Pseudomonas syringae, using a search for genes that resembled those that other bacteria use for directional movement. Our experiments demonstrated that one of these genes is necessary for movement and disease. This is important information because it gives scientists and engineers the identity of the gene responsible for controlling directed movement and provides them with a target to inactivate when designing new ways to control or prevent plant disease. The gene that was found also seems to be changing faster than the majority of genes in the bacterium. Finding a gene that is changing rapidly is important because it suggests that these bacteria somehow benefit from having different versions of that gene. This type of information is important for understanding which gene changes cause bacteria to become more aggressive or more destructive plant pathogens.

Technical Abstract: The majority of bacterial foliar plant pathogens must invade the apoplast of host plants through points of ingress, such as stomata or wounds, replicate to high population density and cause disease. How pathogens navigate plant surfaces to locate invasion sites remains poorly understood. Many bacteria use chemical-directed regulation of flagella, a process known as chemotaxis, to move towards favorable environmental conditions. Chemotactic sensing of the plant surface is a potential mechanism through which foliar plant pathogens hone in on wounds or stomata, but chemotactic systems in foliar plant pathogens are poorly characterized. Comparative genomics of the plant pathogen Pseudomonas syringae pathovar tomato (Pto) implicated annotated chemotaxis genes in the recent adaptations of one Pto lineage. We therefore characterized the chemosensory system of Pto. The Pto genome contains two primary chemotaxis gene clusters, che1 and che2. The che2 cluster is flanked by flagellar biosynthesis genes and similar to the canonical chemotaxis gene clusters of other bacteria based on sequence and synteny. Disruption of the primary phosphorelay kinase gene of the che2 cluster, cheA2, eliminated swimming motility and swarming motility at low temperatures for Pto. The che1 cluster is located next to Type IV pili biosynthesis genes but disruptions in cheA1 has no observable effect on swarming or twitching motility for Pto. Disruption of cheA2 also alters in planta fitness of the pathogen with strains lacking functional cheA2 being less fit in host plants but more fit in a non-host interaction.