Co‐regulation of motility, exoenzyme and antibiotic production by the EnvZ‐OmpR‐FlhDC‐FliA pathway in <i>Xenorhabdus nematophila</i>

Park, Dong-Jin; Forst, Steven

doi:10.1111/j.1365-2958.2006.05320.x

Cited by 76 publications

(140 citation statements)

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“…It is likely that the genes involved in type 1 pili synthesis and other adhesion/invasion factors are controlled at the transcription level by FliA. Although the involvement of FliA in the regulation of virulence determinants other than flagella has been described in several pathogenic bacteria (18,25,26,28), these studies did not identify intermediate steps linking FliA to the regulation of virulence determinants. In our study, we identified the FliA-dependent yhjH gene as such a mediator.…”

Section: Discussionmentioning

confidence: 50%

“…Fig. 1 legend. the Adhesion/Invasion Defect in the ⌬fliA Mutant-To identify putative mediators of the effect of FliA on the synthesis of type 1 pili in strain LF82, we investigated the involvement of two genes, fliZ, which belongs to the fliAZ operon, and yhjH, whose expression depends on FliA in E. coli K-12 and S. typhimurium (25,39). FliZ exerts a control checkpoint between the synthesis of flagella and invasion factors in S. typhimurium (40).…”

Section: Flia Restores Adhesion/invasion Defects In Both ⌬Flia and ⌬Flhdmentioning

confidence: 99%

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The Flagellar Sigma Factor FliA Regulates Adhesion and Invasion of Crohn Disease-associated Escherichia coli via a Cyclic Dimeric GMP-dependent Pathway

Claret

Miquel

Vieille

et al. 2007

Journal of Biological Chemistry

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The invasion of intestinal epithelial cells by the Crohn disease-associated adherent-invasive Escherichia coli (AIEC) strain LF82 depends on surface appendages, such as type 1 pili and flagella. The absence of flagella in the AIEC strain LF82 results in a concomitant loss of type 1 pili. Here, we show that flagellar regulators, transcriptional activator FlhD 2 C 2 , and sigma factor FliA are involved in the coordination of flagellar and type 1 pili synthesis. In the deletion mutants lacking these regulators, type 1 pili synthesis, adhesion, and invasion were severely decreased. FliA expressed alone in trans was sufficient to restore these defects in both the LF82-⌬flhD and LF82-⌬fliA mutants. We related the loss of type 1 pili to the decreased expression of the FliA-dependent yhjH gene in the LF82-⌬fliA mutant. YhjH is an EAL domain phosphodiesterase involved in degradation of the bacterial second messenger cyclic dimeric GMP (c-di-GMP). Increased expression of either yhjH or an alternative c-di-GMP phosphodiesterase, yahA, partially restored type 1 pili synthesis, adhesion, and invasion in the LF82-⌬fliA mutant. Deletion of the GGDEF domain diguanylate cyclase gene, yaiC, involved in c-di-GMP synthesis in the LF82-⌬fliA mutant also partially restored these defects, whereas overexpression of the c-di-GMP receptor YcgR had the opposite effect. These findings show that in the AIEC strain LF82, FliA is a key regulatory component linking flagellar and type 1 pili synthesis and that its effect on type 1 pili is mediated, at least in part, via a c-di-GMP-dependent pathway.Many virulent bacteria, including Aeromonas caviae (1), Campylobacter jejuni (2), Clostridium difficile (3), Helicobacter pylori (4), Legionella pneumophila (5), Salmonella enterica serovar Typhimurium (6), and Vibrio cholerae (7), use flagellar motility to avoid unfavorable environments and to establish replication niches at different stages of infection. In Enterobacteriaceae, flagellar type III secretion and assembly are strictly dependent on the organization of a hierarchy that controls the sequential expression of structural and regulatory genes. In Escherichia coli and Salmonella typhimurium, the heterotetrameric transcription factor FlhD 2 C 2 (8) is positioned at the top of the flagellar expression hierarchy, where the decision to produce flagella is made (9, 10). The flhDC operon encoding FlhD 2 C 2 is transcribed from a class 1 flagellar promoter. FlhD 2 C 2 , in turn, activates 70 -dependent transcription from the class 2 flagellar promoters that drive expression of the structural subunits required for the hook-basal body structure and expression of regulatory subunits (10, 11). One of these regulatory subunits, 28 or FliA, is encoded by the fliAZ operon. FliA can associate with the core RNA polymerase to drive transcription of the class 3 flagellar genes (12). The activity of FliA depends on its interaction with the cytoplasmic anti-sigma factor FlgM, which inhibits the FliA-RNA polymerase association until completion of the hook-basal bo...

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Section: Discussionmentioning

confidence: 50%

Section: Flia Restores Adhesion/invasion Defects In Both ⌬Flia and ⌬Flhdmentioning

confidence: 99%

The Flagellar Sigma Factor FliA Regulates Adhesion and Invasion of Crohn Disease-associated Escherichia coli via a Cyclic Dimeric GMP-dependent Pathway

Claret

Miquel

Vieille

et al. 2007

Journal of Biological Chemistry

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“…We do not yet know whether the same compound is involved in the inhibition of both swarming and catabolism of mucus components. However, if this were the case, it is possible to hypothesize that a higher-level regulatory system (GacS/GacA-Csr or FlhDC) (Romeo, 1998;Pruss et al, 2003;Park and Forst, 2006;Timmermans and Van Melderen, 2010) may be the target. The GacS/GacA-Csr system is not likely to be affected by the activities of these commensals: first, the phenotype of the gacA mutant (Krediet et al, in review) is distinct from what is observed when the wild type is exposed to the commensals tested here, and, second, the commensals did not affect the expression of the gacA::lacZ reporter (Krediet, unpublished data).…”

Section: Discussionmentioning

confidence: 99%

“…Swarming is often coregulated with certain metabolic pathways (Toguchi et al, 2000;Wang et al, 2004). Global regulatory networks (GacS/GacA-Csr, FlhDC-FliA and EnvZ/OmpR) contribute to the control of both the motility and catabolism of specific carbon sources (Park and Forst, 2006;Jones et al, 2008a;Timmermans and Van Melderen, 2010). This coregulation may be instrumental for the regulatory switch that contributes to the efficient establishment within a particular niche.…”

Section: Introductionmentioning

confidence: 99%

Members of native coral microbiota inhibit glycosidases and thwart colonization of coral mucus by an opportunistic pathogen

et al. 2012

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The outcome of the interactions between native commensal microorganisms and opportunistic pathogens is crucial to the health of the coral holobiont. During the establishment within the coral surface mucus layer, opportunistic pathogens, including a white pox pathogen Serratia marcescens PDL100, compete with native bacteria for available nutrients. Both commensals and pathogens employ glycosidases and N-acetyl-glucosaminidase to utilize components of coral mucus. This study tested the hypothesis that specific glycosidases were critical for the growth of S. marcescens on mucus and that their inhibition by native coral microbiota reduces fitness of the pathogen. Consistent with this hypothesis, a S. marcescens transposon mutant with reduced glycosidase and N-acetyl-glucosaminidase activities was unable to compete with the wild type on the mucus of the host coral Acropora palmata, although it was at least as competitive as the wild type on a minimal medium with glycerol and casamino acids. Virulence of the mutant was modestly reduced in the Aiptasia model. A survey revealed that B8% of culturable coral commensal bacteria have the ability to inhibit glycosidases in the pathogen. A small molecular weight, ethanol-soluble substance(s) produced by the coral commensal Exiguobacterium sp. was capable of the inhibition of the induction of catabolic enzymes in S. marcescens. This inhibition was in part responsible for the 10-100-fold reduction in the ability of the pathogen to grow on coral mucus. These results provide insight into potential mechanisms of commensal interference with early colonization and infection behaviors in opportunistic pathogens and highlight an important function for the native microbiota in coral health.

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“…Finally, molecules produced by Xenorhabdus bacteria may themselves be preadaptive signals. Xenorhabdus secondary metabolites are produced during the reproductive phase of the life cycle and can antagonize invading microbial species to protect the insect cadaver (50,57). Changes in the local concentrations of these metabolites could be indicative of conditions that warrant IJ development and emergence.…”

Section: From the Spent Cadaver To The Ijmentioning

confidence: 99%

Ready or Not: Microbial Adaptive Responses in Dynamic Symbiosis Environments

Cao

Goodrich‐Blair

2017

J Bacteriol

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In mutually beneficial and pathogenic symbiotic associations, microbes must adapt to the host environment for optimal fitness. Both within an individual host and during transmission between hosts, microbes are exposed to temporal and spatial variation in environmental conditions. The phenomenon of phenotypic variation, in which different subpopulations of cells express distinctive and potentially adaptive characteristics, can contribute to microbial adaptation to a lifestyle that includes rapidly changing environments. The environments experienced by a symbiotic microbe during its life history can be erratic or predictable, and each can impact the evolution of adaptive responses. In particular, the predictability of a rhythmic or cyclical series of environments may promote the evolution of signal transduction cascades that allow preadaptive responses to environments that are likely to be encountered in the future, a phenomenon known as adaptive prediction. In this review, we summarize environmental variations known to occur in some well-studied models of symbiosis and how these may contribute to the evolution of microbial population heterogeneity and anticipatory behavior. We provide details about the symbiosis between Xenorhabdus bacteria and Steinernema nematodes as a model to investigate the concept of environmental adaptation and adaptive prediction in a microbial symbiosis.

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Co‐regulation of motility, exoenzyme and antibiotic production by the EnvZ‐OmpR‐FlhDC‐FliA pathway in Xenorhabdus nematophila

Cited by 76 publications

References 67 publications

The Flagellar Sigma Factor FliA Regulates Adhesion and Invasion of Crohn Disease-associated Escherichia coli via a Cyclic Dimeric GMP-dependent Pathway

The Flagellar Sigma Factor FliA Regulates Adhesion and Invasion of Crohn Disease-associated Escherichia coli via a Cyclic Dimeric GMP-dependent Pathway

Members of native coral microbiota inhibit glycosidases and thwart colonization of coral mucus by an opportunistic pathogen

Ready or Not: Microbial Adaptive Responses in Dynamic Symbiosis Environments

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