ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae
In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon...
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| Autor*in: |
Li, Caiyi C. [verfasserIn] Merrell, D. Scott [verfasserIn] Camilli, Andrew [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2002 |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Molecular microbiology - Oxford [u.a.] : Wiley-Blackwell, 1987, 43(2002), 6, Seite 0 |
| Übergeordnetes Werk: |
volume:43 ; year:2002 ; number:6 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.1365-2958.2002.02845.x |
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| 520 | |a In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. | ||
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10.1046/j.1365-2958.2002.02845.x doi (DE-627)NLEJ24355866X DE-627 ger DE-627 rakwb Li, Caiyi C. verfasserin aut ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Merrell, D. Scott verfasserin aut Camilli, Andrew verfasserin aut Kaper, James B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 43(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:43 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2958.2002.02845.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 43 2002 6 0 |
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10.1046/j.1365-2958.2002.02845.x doi (DE-627)NLEJ24355866X DE-627 ger DE-627 rakwb Li, Caiyi C. verfasserin aut ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Merrell, D. Scott verfasserin aut Camilli, Andrew verfasserin aut Kaper, James B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 43(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:43 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2958.2002.02845.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 43 2002 6 0 |
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10.1046/j.1365-2958.2002.02845.x doi (DE-627)NLEJ24355866X DE-627 ger DE-627 rakwb Li, Caiyi C. verfasserin aut ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Merrell, D. Scott verfasserin aut Camilli, Andrew verfasserin aut Kaper, James B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 43(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:43 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2958.2002.02845.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 43 2002 6 0 |
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10.1046/j.1365-2958.2002.02845.x doi (DE-627)NLEJ24355866X DE-627 ger DE-627 rakwb Li, Caiyi C. verfasserin aut ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Merrell, D. Scott verfasserin aut Camilli, Andrew verfasserin aut Kaper, James B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 43(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:43 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2958.2002.02845.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 43 2002 6 0 |
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10.1046/j.1365-2958.2002.02845.x doi (DE-627)NLEJ24355866X DE-627 ger DE-627 rakwb Li, Caiyi C. verfasserin aut ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae Oxford, UK Blackwell Science Ltd 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Merrell, D. Scott verfasserin aut Camilli, Andrew verfasserin aut Kaper, James B. oth In Molecular microbiology Oxford [u.a.] : Wiley-Blackwell, 1987 43(2002), 6, Seite 0 Online-Ressource (DE-627)NLEJ243926537 (DE-600)1501537-3 1365-2958 nnns volume:43 year:2002 number:6 pages:0 http://dx.doi.org/10.1046/j.1365-2958.2002.02845.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 43 2002 6 0 |
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ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae |
| abstract |
In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. |
| abstractGer |
In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. |
| abstract_unstemmed |
In pathogenic Vibrio cholerae, the transmembrane DNA-binding protein ToxR co-ordinates the expression of over 20 genes, including those encoding important virulence factors such as cholera toxin and the toxin-co-regulated pilus. The outer membrane protein OmpT is the only member of the ToxR regulon known to be repressed by ToxR. In this study, we examined the environmental conditions that regulate OmpT expression and demonstrated that ompT transcription is upregulated 14-fold when the bacteria enter late log phase from early log phase. Deletion of the crp gene completely abolishes OmpT expression. Comparison of ompT transcription levels in the isogenic crp−, toxR− and crp−toxR− mutants revealed that (i) in the absence of ToxR, constitutive high-level ompT transcription is dependent on cAMP receptor protein (CRP); (ii) ToxR not only interferes with CRP-dependent ompT activation, but also abolishes the CRP-independent, basal level ompT transcription; thus, the mechanism by which ToxR represses ompT transcription involves both antiactivation and direct repression; (iii) both CRP and ToxR are required for the regulation of OmpT expression by growth phase. To provide further insights into the molecular mecha-nism of CRP-dependent activation of ompT transcription, we demonstrated that CRP-dependent activation requires a CRP binding site centred at −310 of the ompT promoter, without which the interaction of CRP with other CRP binding site(s) more proximal to the promoter results in repression. Mutations in two regions on CRP (AR1 and AR2) that directly contact RNA polymerase (RNAP) abolish activation, suggesting direct interaction of CRP with RNAP from −310 of the ompT promoter via DNA looping. |
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6 |
| title_short |
ToxR interferes with CRP-dependent transcriptional activation of ompT in Vibrio cholerae |
| url |
http://dx.doi.org/10.1046/j.1365-2958.2002.02845.x |
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| author2 |
Merrell, D. Scott Camilli, Andrew Kaper, James B. |
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Merrell, D. Scott Camilli, Andrew Kaper, James B. |
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| doi_str |
10.1046/j.1365-2958.2002.02845.x |
| up_date |
2024-07-06T05:50:19.052Z |
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