The production of virulence factors including cholera toxin and the toxin-coregulated pilus in the human pathogen Vibrio cholerae is strongly influenced by environmental conditions. The well-characterized ToxR signal transduction cascade is responsible for sensing and integrating the environmental information and controlling the virulence regulon. We show here that, in addition to the known components of the ToxR signaling circuit, quorum-sensing regulators are involved in regulation of V. cholerae virulence. We focused on the regulators LuxO and HapR because homologues of these two proteins control quorum sensing in the closely related luminous marine bacterium Vibrio harveyi. Using an infant mouse model, we found that a luxO mutant is severely defective in colonization of the small intestine. Gene arrays were used to profile transcription in the V. cholerae wild type and the luxO mutant. These studies revealed that the ToxR regulon is repressed in the luxO mutant, and that this effect is mediated by another negative regulator, HapR. We show that LuxO represses hapR expression early in log-phase growth, and constitutive expression of hapR blocks ToxR-regulon expression. Additionally, LuxO and HapR regulate a variety of other cellular processes including motility, protease production, and biofilm formation. Together these data suggest a role for quorum sensing in modulating expression of blocks of virulence genes in a reciprocal fashion in vivo. The Gram-negative bacterium Vibrio cholerae usually inhabits natural aquatic environments, but it is best known as the causative agent of cholera, a severe diarrheal disease (1). Two factors are critical to V. cholerae virulence-cholera enterotoxin (CT) and an intestinal colonization factor known as the toxincoregulated pilus (TCP). Poorly characterized environmental cues influence the expression of CT and TCP in vivo (2). Two sensory proteins, ToxR and TcpP, likely play a role in detection of the environmental signals, and then initiate a signal transduction cascade that promotes the expression of ToxT, which in turn, directly activates the transcription of genes involved in TCP and CT expression (3).Recent work has established that many species of bacteria monitor their cell-population densities through the exchange of chemical signaling molecules (called autoinducers) that accumulate extracellularly and trigger alterations in behavior at high population densities. This phenomenon is referred to as quorum sensing (4, 5). Quorum sensing controls processes that include bioluminescence, virulence, biofilm formation, and sporulation in various bacterial species. In general, quorum sensing regulates processes that are effective only when a population of bacteria acts in a coordinated manner, but not when the bacteria act as individuals. Gram-negative bacteria typically use acylhomoserine lactones as autoinducers (5, 6), whereas Grampositive bacteria usually use modified oligopeptides as the communication signals (5-7). A link between quorum sensing and virulence has been es...

Vibrio cholerae is the causative agent of the diarrheal disease cholera. By an incompletely understood developmental process, V. cholerae forms complex surface-associated communities called biofilms. Here we show that quorum sensing-deficient mutants of V. cholerae produce thicker biofilms than those formed by wild-type bacteria. Microarray analysis of biofilm-associated bacteria shows that expression of the Vibrio polysaccharide synthesis (vps) operons is enhanced in hapR mutants. CqsA, one of two known autoinducer synthases in V. cholerae, acts through HapR to repress vps gene expression. Vibrio biofilms are more acid resistant than planktonic cells. However, quorum sensing-deficient biofilms have lower colonization capacities than those of wild-type biofilms, suggesting that quorum sensing may promote cellular exit from the biofilm once the organisms have traversed the gastric acid barrier of the stomach. These results shed light on the relationships among biofilm development, quorum sensing, infectivity, and pathogenesis in V. cholerae.

Rhizoctonia solani is a major fungal pathogen of rice (Oryza sativa L.) that causes great yield losses in all rice-growing regions of the world. Here we report the draft genome sequence of the rice sheath blight disease pathogen, R. solani AG1 IA, assembled using next-generation Illumina Genome Analyser sequencing technologies. The genome encodes a large and diverse set of secreted proteins, enzymes of primary and secondary metabolism, carbohydrate-active enzymes, and transporters, which probably reflect an exclusive necrotrophic lifestyle. We find few repetitive elements, a closer relationship to Agaricomycotina among Basidiomycetes, and expand protein domains and families. Among the 25 candidate pathogen effectors identified according to their functionality and evolution, we validate 3 that trigger crop defence responses; hence we reveal the exclusive expression patterns of the pathogenic determinants during host infection.