A σ
            <sup>28</sup>
            -Regulated Nonflagella Gene Contributes to Virulence of
            <i>Campylobacter jejuni</i>
            81-176

Goon, Scarlett; Ewing, Cheryl P.; Lorenzo, María; Pattarini, Dawn; Majam, Gary; Guerry, Patricia

doi:10.1128/iai.74.1.769-772.2006

Cited by 49 publications

(68 citation statements)

References 39 publications

(31 reference 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%

“…These flagellar regulators have been shown to affect the synthesis of virulence factors, directly and indirectly, such as secreted hemolysin in Proteus mirabilis (19), the type III secretion system-1 in Salmonella (20), the Lap phospholipase in Y. enterocolitica (21)(22)(23), an exoenzyme in Xenorhabdus nematophila (24,25), an invasion factor in C. jejuni (26), and factors involved in the intracellular growth of L. pneumophila in amoebas and determinants for the cytotoxicity against macrophages (27,28). Together, these findings indicate that coordinated regulation of motility and virulence factor synthesis is not limited to Enterobacteriaceae.…”

mentioning

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%

mentioning

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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“…Deletion of Cj0256 results in decreased motility and an approximately 95% reduction in flagella production, suggesting that modification of FlgG with pEtN may impart structural stability between the FlgG subunits. Similarly, it has been proposed that glycosylation of filament proteins may provide additional stability to the flagellar filament (25,26). Still, it is not possible to rule out that Cj0256 modifies other targets that play a role in flagellar assembly.…”

Section: Discussionmentioning

confidence: 99%

A link between the assembly of flagella and lipooligosaccharide of the Gram-negative bacterium Campylobacter jejuni

Cullen

Trent

2010

Proc. Natl. Acad. Sci. U.S.A.

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Campylobacter jejuni is the leading cause of acute bacterial diarrhea worldwide and is implicated in development of Guillain-Barré syndrome. Two major surface features, the outer membrane lipooligosaccharide and flagella, are highly variable and are often targets for modification. Presumably, these modifications provide a competitive advantage to the bacterium. In this work, we identify a gene encoding a phosphoethanolamine (pEtN) transferase (Cj0256) that serves a dual role in modifying not only the lipooligosaccharide lipid anchor lipid A with pEtN, but also the flagellar rod protein FlgG. Generation of a mutant in C. jejuni 81-176 by interruption of cj0256 resulted in the absence of pEtN modifications on lipid A as well as FlgG. The cj0256 mutant showed a 20-fold increase in sensitivity to the cationic antimicrobial peptide, polymyxin B, as well as a decrease in motility. Transmission EM of the cj0256 mutant revealed a population (approximately 95%) lacking flagella, indicating that, without pEtN modification of FlgG, flagella production is hindered. Most intriguing, this research identifies a pEtN transferase showing preference for two periplasmic substrates linking membrane biogenesis and flagellar assembly. Cj0256 is a member of a large family of mostly uncharacterized proteins that may play a larger role in the decoration of bacterial surface structures.

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“…Unlike Salmonella spp., which use T3SSs and translocated effector proteins to manipulate host cells for invasion and intracellular survival, C. jejuni lacks genes encoding these virulence factors. Instead, C. jejuni is thought to take advantage of the flagellar T3SS to secrete potential effector proteins that may assist in invasion and intracellular survival processes (217,339,559).…”

Section: Invasion Of Intestinal Epithelium and Intracellular Replicationmentioning

confidence: 99%

“…Also potentially included as class 2 genes are fliA and flgM, which encode 28 and its anti-factor, since some evidence exists that expression of these genes is partially 54 dependent (80,650). Class 3 genes include those dependent on 28 for expression, which include flaA, genes encoding minor filament proteins, and a few nonflagellar genes that may encode proteins involved in virulence mechanisms (217,489). This transcriptional hierarchy accounts for the requirement of two alternative factors for tight and ordered control of flagellar genes for proper biosynthesis of the flagellar organelle.…”

Section: Transcriptional Regulatory Cascades For Flagellar Gene Exprementioning

confidence: 99%

Change Is Good: Variations in Common Biological Mechanisms in the Epsilonproteobacterial GeneraCampylobacterandHelicobacter

Gilbreath

Cody

Merrell

et al. 2011

Microbiol Mol Biol Rev

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SUMMARY Microbial evolution and subsequent species diversification enable bacterial organisms to perform common biological processes by a variety of means. The epsilonproteobacteria are a diverse class of prokaryotes that thrive in diverse habitats. Many of these environmental niches are labeled as extreme, whereas other niches include various sites within human, animal, and insect hosts. Some epsilonproteobacteria, such as Campylobacter jejuni and Helicobacter pylori , are common pathogens of humans that inhabit specific regions of the gastrointestinal tract. As such, the biological processes of pathogenic Campylobacter and Helicobacter spp. are often modeled after those of common enteric pathogens such as Salmonella spp. and Escherichia coli . While many exquisite biological mechanisms involving biochemical processes, genetic regulatory pathways, and pathogenesis of disease have been elucidated from studies of Salmonella spp. and E. coli , these paradigms often do not apply to the same processes in the epsilonproteobacteria. Instead, these bacteria often display extensive variation in common biological mechanisms relative to those of other prototypical bacteria. In this review, five biological processes of commonly studied model bacterial species are compared to those of the epsilonproteobacteria C. jejuni and H. pylori . Distinct differences in the processes of flagellar biosynthesis, DNA uptake and recombination, iron homeostasis, interaction with epithelial cells, and protein glycosylation are highlighted. Collectively, these studies support a broader view of the vast repertoire of biological mechanisms employed by bacteria and suggest that future studies of the epsilonproteobacteria will continue to provide novel and interesting information regarding prokaryotic cellular biology.

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A σ ²⁸ -Regulated Nonflagella Gene Contributes to Virulence of Campylobacter jejuni 81-176

Cited by 49 publications

References 39 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

A link between the assembly of flagella and lipooligosaccharide of the Gram-negative bacterium Campylobacter jejuni

Change Is Good: Variations in Common Biological Mechanisms in the Epsilonproteobacterial GeneraCampylobacterandHelicobacter

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A σ 28 -Regulated Nonflagella Gene Contributes to Virulence of Campylobacter jejuni 81-176

Cited by 49 publications

References 39 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

A link between the assembly of flagella and lipooligosaccharide of the Gram-negative bacterium Campylobacter jejuni

Change Is Good: Variations in Common Biological Mechanisms in the Epsilonproteobacterial GeneraCampylobacterandHelicobacter

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A σ ²⁸ -Regulated Nonflagella Gene Contributes to Virulence of Campylobacter jejuni 81-176