1.5.3S
WHAT'S GOING ON OUT THERE? ENVIRONMENTAL SENSING AND CONTROL OF VIRULENCE GENES IN RALSTONIA SOLANACEARUM

MA SCHELL, A FLAVIER, TP DENNY, J McGARVEY, W YINDEEYOUNGYEON and Y KANG

Departments of Microbiology and Plant Pathology, University of Georgia, Athens, GA 30602, USA

Ralstonia (Pseudomonas) solanacearum causes a lethal wilting disease of over 200 different plants around the world. It secretes multiple plant cell wall-degrading exoenzymes and the exopolysaccharide EPS 1, all of which are important for its rapid colonization of the vascular system after root invasion. Production of large amounts of EPS 1 is also the primary cause of wilting (and killing) of infected plants due to its ability to block water flow in the xylem. Transcription of eps, the operon encoding the biosynthetic pathway for EPS 1 as well as many other virulence genes, is controlled by a extensive, interactive regulatory network comprising at least 12 proteins and responsive to multiple environmental signals [1]. The network uses at least four distinct two­component regulatory systems to coordinate and communicate important information about the pathogen's environment to virulence gene promoters in order to modulate their transcription by RNA polymerase. One of the most critical genes for virulence of R. solanacearum is the network component PhcA, a LysR-type transcriptional regulator that globally alters the expression of many genes. When PhcA becomes active, it causes a dramatic and reversible switch in the physiological status of R. solanacearum from one specialized for saprophytic soil survival to one that is highly adapted for virulence in plants. Experiments describing control of PhcA activity by a novel phospho-relay cascade and a new type of volatile, quorum or confinement-sensing molecule [2] will be discussed, as will data demonstrating that PhcA controls the activation of a second quorum-sensing system of the classic homoserine lactone (auto-inducer) type just prior to the entrance into stationary phase [3]. Recent investigations of the protein-DNA and protein-protein interactions that occur between network components to integrate multiple signal inputs, and thus allow control of virulence gene transcription in simultaneous response to four independent signals, will also be presented. Finally, discovery and analysis of new target genes regulated by the network will be discussed.

References
1. Schell MA, 1996. European Journal of Plant Pathology 102, 459-469.
2. Clough SJ, Schell, MA, Denny TP, 1997. Journal of Bacteriology 179, 3639-3648.
3. Flavier AB, Ganova-Raeva L, Schell MA, Denny TP, 1997. Journal of Bacteriology 179, 7089-7099.