culture desulfovibrio vulgaris  (ATCC)


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    ATCC culture desulfovibrio vulgaris
    Culture Desulfovibrio Vulgaris, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    postgate b medium a pure culture srb desulfovibrio vulgaris  (ATCC)


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    ATCC postgate b medium a pure culture srb desulfovibrio vulgaris
    Postgate B Medium A Pure Culture Srb Desulfovibrio Vulgaris, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    desulfovibrio vulgaris  (ATCC)


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    ATCC desulfovibrio vulgaris
    Desulfovibrio Vulgaris, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    dvf desulfovibrio vulgaris flagellin lrrc19 leucine  (ATCC)


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    ATCC dvf desulfovibrio vulgaris flagellin lrrc19 leucine
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    GenScript corporation desulfovibrio vulgaris
    Desulfovibrio Vulgaris, supplied by GenScript corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    desulfovibrio vulgaris subsp vulgaris postgate  (ATCC)


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    ATCC desulfovibrio vulgaris subsp vulgaris postgate
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    desulfovibrio vulgaris  (ATCC)


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    ATCC desulfovibrio vulgaris
    a) T1SS in Pseudomonas fluorescens Pf0-1. The large adhesin LapA is localized to the outer membrane (OM) via a retention module, allowing the bacterium to form a biofilm. The localization of LapA to the OM is regulated by a periplasmic protease LapG and a cyclic di-GMP (cdG) effector protein LapD. At high intracellular cdG levels, the catalytically inactive EAL domain of LapD binds cdG leading to a conformational change whereby the LapD periplasmic domain sequesters LapG, thereby retaining LapA on the OM. When c-di-GMP levels are low, LapD is in its autoinhibited conformation, which releases LapG to cleave LapA at dialanine motif (shown in red), resulting in the release of LapA to the extracellular environment and loss of biofilm formation. b) Proposed model of T1SS in <t>Desulfovibrio</t> <t>vulgaris</t> Hildenborough. DvhA is a LapA-like adhesin localized to the OM. DvhG is a LapG-like protease that can cleave DvhA at the dialanine site (shown in red), however, unlike the periplasmic-localized LapG, DvhG is hypothesized to be inner membrane (IM) bound. DvhD is a structurally different but functionally analogous LapD-like protein containing a catalytically inactive HD-GYP domain that can bind c-di-GMP and thus regulate DvhA localization and biofilm formation in D. vulgaris Hildenborough. c) Simplified protein architecture representing different domains and the dialanine site of Pf0-1 adhesin LapA, DvH adhesin DvhA and fusion proteins DvhA-RM-swap and DvhA-hlx-swap (RM - retention module; polyG – polyglycine linker; SD – C-terminal secretion domain). Protein domains are not to scale. d) Biofilm formed in K10T medium at 24 hours by strains expressing the adhesins DvhA-RM-swap and DvhA-hlx-swap compared to the native adhesin LapA in Pf0-1, all in the Δ lapG Δ lapD background strain. e) Quantification of cell surface levels of HA-tagged adhesins at 24 hours in K10T medium. f) Western blots indicating total cellular levels of the different adhesins. Statistical analysis was performed using one way ANOVA multiple comparisons (ns, p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001); ****, P<0.0001).
    Desulfovibrio Vulgaris, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Reconstitution of a Biofilm Adhesin System from a Sulfate-Reducing Bacterium in Pseudomonas fluorescens"

    Article Title: Reconstitution of a Biofilm Adhesin System from a Sulfate-Reducing Bacterium in Pseudomonas fluorescens

    Journal: bioRxiv

    doi: 10.1101/2023.11.22.568322

    a) T1SS in Pseudomonas fluorescens Pf0-1. The large adhesin LapA is localized to the outer membrane (OM) via a retention module, allowing the bacterium to form a biofilm. The localization of LapA to the OM is regulated by a periplasmic protease LapG and a cyclic di-GMP (cdG) effector protein LapD. At high intracellular cdG levels, the catalytically inactive EAL domain of LapD binds cdG leading to a conformational change whereby the LapD periplasmic domain sequesters LapG, thereby retaining LapA on the OM. When c-di-GMP levels are low, LapD is in its autoinhibited conformation, which releases LapG to cleave LapA at dialanine motif (shown in red), resulting in the release of LapA to the extracellular environment and loss of biofilm formation. b) Proposed model of T1SS in Desulfovibrio vulgaris Hildenborough. DvhA is a LapA-like adhesin localized to the OM. DvhG is a LapG-like protease that can cleave DvhA at the dialanine site (shown in red), however, unlike the periplasmic-localized LapG, DvhG is hypothesized to be inner membrane (IM) bound. DvhD is a structurally different but functionally analogous LapD-like protein containing a catalytically inactive HD-GYP domain that can bind c-di-GMP and thus regulate DvhA localization and biofilm formation in D. vulgaris Hildenborough. c) Simplified protein architecture representing different domains and the dialanine site of Pf0-1 adhesin LapA, DvH adhesin DvhA and fusion proteins DvhA-RM-swap and DvhA-hlx-swap (RM - retention module; polyG – polyglycine linker; SD – C-terminal secretion domain). Protein domains are not to scale. d) Biofilm formed in K10T medium at 24 hours by strains expressing the adhesins DvhA-RM-swap and DvhA-hlx-swap compared to the native adhesin LapA in Pf0-1, all in the Δ lapG Δ lapD background strain. e) Quantification of cell surface levels of HA-tagged adhesins at 24 hours in K10T medium. f) Western blots indicating total cellular levels of the different adhesins. Statistical analysis was performed using one way ANOVA multiple comparisons (ns, p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001); ****, P<0.0001).
    Figure Legend Snippet: a) T1SS in Pseudomonas fluorescens Pf0-1. The large adhesin LapA is localized to the outer membrane (OM) via a retention module, allowing the bacterium to form a biofilm. The localization of LapA to the OM is regulated by a periplasmic protease LapG and a cyclic di-GMP (cdG) effector protein LapD. At high intracellular cdG levels, the catalytically inactive EAL domain of LapD binds cdG leading to a conformational change whereby the LapD periplasmic domain sequesters LapG, thereby retaining LapA on the OM. When c-di-GMP levels are low, LapD is in its autoinhibited conformation, which releases LapG to cleave LapA at dialanine motif (shown in red), resulting in the release of LapA to the extracellular environment and loss of biofilm formation. b) Proposed model of T1SS in Desulfovibrio vulgaris Hildenborough. DvhA is a LapA-like adhesin localized to the OM. DvhG is a LapG-like protease that can cleave DvhA at the dialanine site (shown in red), however, unlike the periplasmic-localized LapG, DvhG is hypothesized to be inner membrane (IM) bound. DvhD is a structurally different but functionally analogous LapD-like protein containing a catalytically inactive HD-GYP domain that can bind c-di-GMP and thus regulate DvhA localization and biofilm formation in D. vulgaris Hildenborough. c) Simplified protein architecture representing different domains and the dialanine site of Pf0-1 adhesin LapA, DvH adhesin DvhA and fusion proteins DvhA-RM-swap and DvhA-hlx-swap (RM - retention module; polyG – polyglycine linker; SD – C-terminal secretion domain). Protein domains are not to scale. d) Biofilm formed in K10T medium at 24 hours by strains expressing the adhesins DvhA-RM-swap and DvhA-hlx-swap compared to the native adhesin LapA in Pf0-1, all in the Δ lapG Δ lapD background strain. e) Quantification of cell surface levels of HA-tagged adhesins at 24 hours in K10T medium. f) Western blots indicating total cellular levels of the different adhesins. Statistical analysis was performed using one way ANOVA multiple comparisons (ns, p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001); ****, P<0.0001).

    Techniques Used: Membrane, Expressing, Western Blot

    a) The gene encoding HA-tagged DvhD gene from D. vulgaris Hildenborough was inserted at the Tn7 att site under the control of IPTG-inducible P tac promoter in the Pf0-1 Δ lapG Δ lapDdvhA-hlx-swap strain. The lacI gene was also introduced at the att site to repress dvhD gene expression in the absence of IPTG. b) Whole-cell western blot for HA-tagged proteins shows minimal DvhD without IPTG and increased DvhD level in the presence of IPTG. c) Biofilm formed by the Pf0-1 attTn7:: lacI P tac dvhD -HA Δ lapG Δ lapDdvhA-hlx-swap strain in K10T medium at 24 hours. Quantification was performed on the strain containing no vector, empty vector and plasmid expressing full length DvhG. Arabinose at 0.2% and IPTG at 0.01% were used to induce dvhG expression from the plasmid and dvhD expression from the genome, respectively. d,e) Quantification of DvhA-hlx-swap on the cell surface (d) and the culture supernatant (e) using dot blots in the presence or absence of IPTG. The analyzed strains carried either an empty vector or a plasmid expressing full length DvhG, all under inducing conditions with 0.2% arabinose. Statistical analysis was performed using one way ANOVA multiple comparisons (ns, p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).
    Figure Legend Snippet: a) The gene encoding HA-tagged DvhD gene from D. vulgaris Hildenborough was inserted at the Tn7 att site under the control of IPTG-inducible P tac promoter in the Pf0-1 Δ lapG Δ lapDdvhA-hlx-swap strain. The lacI gene was also introduced at the att site to repress dvhD gene expression in the absence of IPTG. b) Whole-cell western blot for HA-tagged proteins shows minimal DvhD without IPTG and increased DvhD level in the presence of IPTG. c) Biofilm formed by the Pf0-1 attTn7:: lacI P tac dvhD -HA Δ lapG Δ lapDdvhA-hlx-swap strain in K10T medium at 24 hours. Quantification was performed on the strain containing no vector, empty vector and plasmid expressing full length DvhG. Arabinose at 0.2% and IPTG at 0.01% were used to induce dvhG expression from the plasmid and dvhD expression from the genome, respectively. d,e) Quantification of DvhA-hlx-swap on the cell surface (d) and the culture supernatant (e) using dot blots in the presence or absence of IPTG. The analyzed strains carried either an empty vector or a plasmid expressing full length DvhG, all under inducing conditions with 0.2% arabinose. Statistical analysis was performed using one way ANOVA multiple comparisons (ns, p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

    Techniques Used: Expressing, Western Blot, Plasmid Preparation

    desulfovibrio vulgaris  (ATCC)


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    ATCC desulfovibrio vulgaris
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    NCIMB Ltd strains desulfovibrio vulgaris ncimb 8303
    Strains Desulfovibrio Vulgaris Ncimb 8303, supplied by NCIMB Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    NCIMB Ltd strains desulfovibrio vulgaris ncimb 8303
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