Quorum Sensing Negatively Regulates Hemolysin Transcriptionally and Posttranslationally in
            <i>Vibrio cholerae</i>

Tsou, Amy M.; Zhu, Jun

doi:10.1128/iai.00590-09

Cited by 54 publications

(49 citation statements)

References 50 publications

(46 reference statements)

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“…It is interesting to note that the predominant role of Dly in the lysis of mouse and turbot erythrocytes prevents us from observing whether this repression also occurs in these two blood types. Recently, it was reported that V. cholerae HlyA hemolysin is negatively regulated via the quorum-sensing-regulated transcription factor HapR, and this negative regulation is exerted at the transcriptional and posttranslational levels (45). We demonstrated, using transcriptional lacZ fusions, that inhibition of HlyA pl in P. damselae subsp.…”

Section: Discussionmentioning

confidence: 97%

Synergistic and Additive Effects of Chromosomal and Plasmid-Encoded Hemolysins Contribute to Hemolysis and Virulence in Photobacterium damselae subsp. damselae

et al. 2013

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Photobacterium damselae subsp. damselae causes infections and fatal disease in marine animals and in humans. Highly hemolytic strains produce damselysin (Dly) and plasmid-encoded HlyA (HlyA pl ). These hemolysins are encoded by plasmid pPHDD1 and contribute to hemolysis and virulence for fish and mice. In this study, we report that all the hemolytic strains produce a hitherto uncharacterized chromosome-encoded HlyA (HlyA ch ). Hemolysis was completely abolished in a single hlyA ch mutant of a plasmidless strain and in a dly hlyA pl hlyA ch triple mutant. We found that Dly, HlyA pl , and HlyA ch are needed for full hemolytic values in strains harboring pPHDD1, and these values are the result of the additive effects between HlyA pl and HlyA ch , on the one hand, and of the synergistic effect of Dly with HlyA pl and HlyA ch , on the other hand. Interestingly, Dly-producing strains produced synergistic effects with strains lacking Dly production but secreting HlyA, constituting a case of the CAMP (Christie, Atkins, and Munch-Petersen) reaction. Environmental factors such as iron starvation and salt concentration were found to regulate the expression of the three hemolysins. We found that the contributions, in terms of the individual and combined effects, of the three hemolysins to hemolysis and virulence varied depending on the animal species tested. While Dly and HlyA pl were found to be main contributors in the virulence for mice, we observed that the contribution of hemolysins to virulence for fish was mainly based on the synergistic effects between Dly and either of the two HlyA hemolysins rather than on their individual effects.

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Section: Discussionmentioning

confidence: 97%

Synergistic and Additive Effects of Chromosomal and Plasmid-Encoded Hemolysins Contribute to Hemolysis and Virulence in Photobacterium damselae subsp. damselae

et al. 2013

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“…Many virulence factors, including cholera toxin, the toxin-coregulated pilus, and the HlyA hemolysin are expressed at a low cell density and then repressed at a high cell density by HapR. However, HapR also positively regulates the expression of other virulence genes, such as the HA/protease and a T6SS, and represses the extracellular polysaccharide locus and biofilm development (29,34,61,(76)(77)(78). The nature of the genes regulated by the central output regulator of the quorum pathway has been examined for a few other Vibrio species.…”

Section: Discussionmentioning

confidence: 99%

Quorum Sensing and Silencing in Vibrio parahaemolyticus

2011

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The quorum regulatory cascade is poorly characterized in Vibrio parahaemolyticus, in part because swarming and virulence factors-the hallmarks of the organism-are repressed by this scheme of gene control, and quorum sensing seems to be silenced in many isolates. In these studies, we examine a swarming-proficient, virulent strain and identify an altered-function allele of the quorum regulator luxO that is demonstrated to produce a constitutively active mimic of LuxOϳP. We find that LuxO* affects the expression of three small regulatory RNAs (Qrrs) and the activity of a translational fusion in opaR, the output regulator. Tests for epistasis showed that luxO* is dominant over luxO and that opaR is dominant over luxO. Thus, information flow through the central elements of the V. parahaemolyticus quorum pathway is proven for the first time. Quorumsensing output was explored using microarray profiling: the OpaR regulon encompasses ϳ5.2% of the genome. OpaR represses the surface-sensing and type III secretion system 1 (T3SS1) regulons. One novel discovery is that OpaR strongly and oppositely regulates two type VI secretion systems (T6SS). New functional consequences of OpaR control were demonstrated: OpaR increases the cellular cyclic di-GMP (c-di-GMP) level, positively controls chitin-induced DNA competency, and profoundly blocks cytotoxicity toward host cells. In expanding the previously known quorum effects beyond the induction of the capsule and the repression of swarming to elucidate the global scope of genes in the OpaR regulon, this study yields many clues to distinguishing traits of this Vibrio species; it underscores the profoundly divergent survival strategies of the quorum On/Off phase variants.Many members of the Vibrionaceae are well known for their capacities to communicate and to control group activities such as biofilm formation, virulence, and luminescence via cell-tocell signaling (reviewed in reference 48). However, quorum sensing has not been intensively investigated in Vibrio parahaemolyticus. This ubiquitous marine organism is the leading worldwide cause of seafood-borne gastroenteritis (43,47,60). Although its pathogenic strategies are not well understood, V. parahaemolyticus possesses a powerful arsenal of potential virulence factors, including proteases, hemolysins, two type VI secretion systems (T6SS1 and T6SS2), and two type III secretion systems (T3SS1 and TSS2) (37). The two T3SS, which are specially designed to inject effector virulence factors into eukaryotic host cells, have garnered much attention recently and have been shown to play distinct and critical roles in the pathogenicity of the organism (9, 27). Another hallmark of the organism is a marked proficiency at surface colonization, which is determined by its vigorous capacity to swarm and form robust biofilms (reviewed in reference 39). Our lack of knowledge about quorum sensing in V. parahaemolyticus stems in part from the fact that the archetypal V. parahaemolyticus strains appear defective in cell density-dependent regulation. S...

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“…There are additional two genes predicted to encode hemolysin-like proteins; however, deletion of these two genes did not affect the hemolytic activity of V. fluvialis (data not shown). In V. cholerae, QS negatively regulates hemolysin gene expression (41). To test whether QS controls hemolysin expression in V. fluvialis, we examined vfh expression in the wild type and QS mutants using qRT-PCR (Fig.…”

Section: Fig 4 Hapr Regulation Of Ahl-vfqr (A) Effect Of Hapr Deletimentioning

confidence: 99%

Quorum Sensing Regulatory Cascades Control Vibrio fluvialis Pathogenesis

Wang

Liang

et al. 2013

J Bacteriol

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c Quorum sensing (QS) is a process by which individual bacteria are able to communicate with one another, thereby enabling the population as a whole to coordinate gene regulation and subsequent phenotypic outcomes. Communication is accomplished through production and detection of small molecules in the extracellular milieu. In many bacteria, particularly Vibrio species, multiple QS systems result in multiple signals, as well as cross talk between systems. In this study, we identify two QS systems in the halophilic enteric pathogen Vibrio fluvialis: one acyl-homoserine lactone (AHL) based and one CAI-1/AI-2 based. We show that a LuxI homolog, VfqI, primarily produces 3-oxo-C10-HSL, which is sensed by a LuxR homolog, VfqR. VfqR-AHL is required to activate vfqI expression and autorepress vfqR expression. In addition, we have shown that similar to that in V. cholerae and V. harveyi, V. fluvialis produces CAI-1 and AI-2 signal molecules to activate the expression of a V. cholerae HapR homolog through LuxO. Although VfqR-AHL does not regulate hapR expression, HapR can repress vfqR transcription. Furthermore, we found that QS in V. fluvialis positively regulates production of two potential virulence factors, an extracellular protease and hemolysin. QS also affects cytotoxic activity against epithelial tissue cultures. These data suggest that V. fluvialis integrates QS regulatory pathways to play important physiological roles in pathogenesis. Bacteria often exchange chemical signals to help them monitor their population densities through a phenomenon referred to as quorum sensing (QS) (1). The genus Vibrio includes more than 30 species, many of which are associated with human diseases, and have described QS systems for both interbacterial and intrabacterial communication (2). Among them, the acyl-homoserine lactone (AHL) system in Vibrio fischeri is well characterized and is used as a model system for many AHL-producing Gram-negative bacteria (3). The AHL signal molecule is produced by the AHL synthase LuxI and recognized by the LuxR receptor, leading to altered gene expression of downstream genes. In Vibrio cholerae, the causative agent of cholera (4), the major QS signal molecules are 3-hydroxytridecan-4-one (cholerae autoinducer-1 [CAI-1]) and AI-2 (5). Changes in these autoinducer levels correspond to repression or derepression of the major QS regulator, HapR. At a low cell density and signal concentration, a phosphorelay system is active, resulting in the phosphorylation of the terminal acceptor LuxO, a DNA-binding response regulator protein. PhosphoLuxO, together with a sigma factor 54 , activates transcription of the genes encoding a set of small RNAs that, in conjunction with RNA chaperone, Hfq, bind to and destabilize the transcript of HapR, the master QS regulator (6). Alternatively, at high cell density, QS molecules interact with their cognate sensors, leading to the dephosphorylation of LuxO. Consequently, LuxO is inactivated and HapR is expressed (7, 8; see also two review articles [9,10] for additional de...

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Quorum Sensing Negatively Regulates Hemolysin Transcriptionally and Posttranslationally in Vibrio cholerae

Cited by 54 publications

References 50 publications

Synergistic and Additive Effects of Chromosomal and Plasmid-Encoded Hemolysins Contribute to Hemolysis and Virulence in Photobacterium damselae subsp. damselae

Synergistic and Additive Effects of Chromosomal and Plasmid-Encoded Hemolysins Contribute to Hemolysis and Virulence in Photobacterium damselae subsp. damselae

Quorum Sensing and Silencing in Vibrio parahaemolyticus

Quorum Sensing Regulatory Cascades Control Vibrio fluvialis Pathogenesis

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