Structural features, properties and regulation of the outer-membrane protein W (OmpW) of Vibrio cholerae

Nandi, Bisweswar; Nandy, Ranjan K.; Sarkar, Amit; Ghose, A.M.

doi:10.1099/mic.0.27995-0

Cited by 102 publications

(97 citation statements)

References 58 publications

(59 reference statements)

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“…3). This was consistent with the results of a previous study that showed the intestinal colonization activities of ompWdeficient mutants to be at only marginally lower levels than those of wild-type O1 strains (9). In this way, ompW mutants were shown to have less adaptability to their environments and to human hosts than their wild-type counterparts.…”

supporting

confidence: 81%

Outer Membrane Protein OmpW Is the Receptor for Typing Phage VP5 in the Vibrio cholerae O1 El Tor Biotype

Zhang

Liu

et al. 2014

J Virol

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Phage typing is used for the subtyping of clones of epidemic bacteria. In this study, we identified the outer membrane protein OmpW as the receptor for phage VP5, one of the typing phages for the Vibrio cholerae O1 El Tor biotype. A characteristic 11-bp deletion in ompW was observed in all epidemic strains resistant to VP5, suggesting that this mutation event can be used as a tracing marker in cholera surveillance. Seven cholera pandemics have been recorded historically. The first six pandemics were putatively caused by the classical biotype of Vibrio cholerae serogroup O1, whereas the ongoing seventh pandemic is caused by the O1 El Tor biotype (1). Subtyping of V. cholerae strains is useful in epidemiological and microbiological studies. A phage-biotyping scheme, in which five typing phages (VP1 to VP5) were included, was established for El Tor strain subtyping in the 1970s in China (2). During surveillance of V. cholerae strains, almost all El Tor strains from epidemics were found to be sensitive to all five of these typing phages and are designated phage type 1 (PT1) strains. However, during the 1998 cholera epidemic in Sichuan Province, some patient strains were resistant to phage VP5. These strains belong to the PT6 group and coexisted with PT1 strains. PT6 strains became predominant in 1999 and 2000 but disappeared after 2001 (3), which makes them unique among the epidemic strains.Phages infect susceptible bacterial strains, beginning with binding to receptors on the surfaces of bacteria. OmpW is an outer membrane protein that serves as a receptor for Escherichia coli colicin S4 (4). The ompW gene has served as a species-specific gene of V. cholerae in many detection studies (5, 6). This gene was found to have an 11-bp deletion in the PT6 strains, but the deletion was not detected in any PT1 strain (3). Therefore, a role for OmpW in VP5 infection was suspected.In this study, ompW genes from 44 strains isolated from 1998 to 2001, including 22 PT6 and 11 PT1 strains from Sichuan and 11 PT1 strains from other provinces, were sequenced. The same 11-bp deletion was in all PT6 strains (Fig. 1). The deletion corresponds to nucleotides (nt) 298 to 308 of ompW and causes a shift in the reading frame. A new stop codon is generated at 350 nt, ahead of the original stop codon (Fig. 1). All the PT1 strains had intact and identical ompW sequences.To assess the possible role of the ompW gene in VP5 infection, we constructed an ompW deletion mutant, designated N16961-dompW, with suicide plasmid pWM91 (7) from the VP5-sensitive strain N16961. The N16961-dompW mutant lost sensitivity to VP5 ( Fig. 2A). This sensitivity was restored when it was complemented with plasmid pBR322-ompW (designated strain N16961-dompW-R) containing the intact ompW gene cloned from N16961 but not when it obtained pBR322-ompW(del) containing ompW with an 11-bp deletion cloned from the PT6 strain VC631. VC631 became sensitive to VP5 when it obtained plasmid pBR322-ompW but remained resistant when it obtained pBR322-ompW(del) ( Fig. 2A), indicating t...

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supporting

confidence: 81%

Outer Membrane Protein OmpW Is the Receptor for Typing Phage VP5 in the Vibrio cholerae O1 El Tor Biotype

Zhang

Liu

et al. 2014

J Virol

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“…2A, we used semiquantitative RT-PCR to measure the vasX transcript levels in the complemented V52⌬vasH strain relative to the transcription of the outer membrane protein OmpW. It was previously demonstrated that the presence of arabinose does not affect the expression of OmpW (30). When vasH expression was induced with arabinose, vasX transcript levels increased ϳ10-fold (Fig.…”

Section: Identification Of Vasxmentioning

confidence: 99%

Vibrio cholerae Requires the Type VI Secretion System Virulence Factor VasX To Kill Dictyostelium discoideum

et al. 2011

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The type VI secretion system (T6SS) is recognized as an important virulence mechanism in several Gram-negative pathogens. In Vibrio cholerae, the causative agent of the diarrheal disease cholera, a minimum of three gene clusters-one main cluster and two auxiliary clusters-are required to form a functional T6SS apparatus capable of conferring virulence toward eukaryotic and prokaryotic hosts. Despite an increasing understanding of the components that make up the T6SS apparatus, little is known about the regulation of these genes and the gene products delivered by this nanomachine. VasH is an important regulator of the V. cholerae T6SS. Here, we present evidence that VasH regulates the production of a newly identified protein, VasX, which in turn requires a functional T6SS for secretion. Deletion of vasX does not affect export or enzymatic function of the structural T6SS proteins Hcp and VgrG-1, suggesting that VasX is dispensable for the assembly of the physical translocon complex. VasX localizes to the bacterial membrane and interacts with membrane lipids. We present VasX as a novel virulence factor of the T6SS, as a V. cholerae mutant lacking vasX exhibits a phenotype of attenuated virulence toward Dictyostelium discoideum.Vibrio cholerae is the marine bacterium responsible for the diarrheal disease cholera. Multiple cholera pandemics have been caused by the O1 serogroup of V. cholerae, and recently, O139 has emerged as a new pandemic strain (11). The principal virulence factors postulated to be essential for the pandemic spread of strains belonging to these serogroups are cholera toxin (CT) and the toxin-coregulated pilus (TCP) (13, 17). Non-O1 and non-O139 serogroups of V. cholerae are also capable of causing disease, in some cases in the absence of CT and TCP (10). In 1968, the O37 serogroup strain V52 was responsible for an outbreak of cholera-like diarrheal illness in Sudan, with 460 cases leading to 125 deaths (42). The genome of V52 carries both CT and TCP genes, but whether this strain produces CT and TCP in vivo has not yet been determined. V52 possesses a constitutively active type VI secretion system (T6SS) that confers virulence toward phagocytic cells, including the social amoeba Dictyostelium discoideum and murine macrophages (34). Pandemic strains of V. cholerae also possess the full complement of T6SS genes, but it is currently unclear how the T6SS is activated and how this system contributes to human disease.

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“…The induced protection against V. cholerae following immunization by 22 kDa ompW protein has been reported to be mediated by the binding of antibodies to this protein, causing V. cholerae immobilization or agglutination. Therefore, these mechanisms interfere with the colonization process that is usually mediated by factors of pilus or non-pilus origin (7). The lipopolysaccharide (LPS) content of V. cholerae, in addition to the ompW protein, has been reported to induce a protective immunity in the host (8).…”

Section: Introductionmentioning

confidence: 99%

Serum Anti-Vibrio cholerae Immunoglobulin Isotype in BALB/c Mice Immunized With ompW-Loaded Chitosan

Fasihi-Ramandi¹,

Ghobadi-Ghadikolaee²,

Ahmadi-Renani³

et al. 2016

Int J Enteric Pathog

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Structural features, properties and regulation of the outer-membrane protein W (OmpW) of Vibrio cholerae

Cited by 102 publications

References 58 publications

Outer Membrane Protein OmpW Is the Receptor for Typing Phage VP5 in the Vibrio cholerae O1 El Tor Biotype

Outer Membrane Protein OmpW Is the Receptor for Typing Phage VP5 in the Vibrio cholerae O1 El Tor Biotype

Vibrio cholerae Requires the Type VI Secretion System Virulence Factor VasX To Kill Dictyostelium discoideum

Serum Anti-Vibrio cholerae Immunoglobulin Isotype in BALB/c Mice Immunized With ompW-Loaded Chitosan

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