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distinct crispr arrays  (ATCC)


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    Structured Review

    ATCC distinct crispr arrays
    Impact of <t>CRISPR</t> array 30.1 deletion on growth, biofilm formation, and virulence of <t>P.</t> <t>gingivalis</t> ATCC 33277. ( a ) Growth curve comparing planktonic growth of wild-type and ΔCRISPR array 30.1 mutant strains. ( b ) Biofilm biomass quantification of wild-type and ΔCRISPR array 30.1 mutant strains grown on microtiter plates, assessed by safranin staining (OD at 492 nm). ( c–e ) Kaplan–Meier survival analysis of Galleria mellonella larvae injected with different concentrations of wild-type or ΔCRISPR array 30.1 mutant strains: ( c ) 6 × 10 7 CFU/mL; ( d ) 3 × 10 8 CFU/mL; and ( e ) 6 × 10 8 CFU/mL. Survival differences between groups were statistically significant ( P < 0.0001). Controls represent larvae injected with PBS only.
    Distinct Crispr Arrays, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 283 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/distinct crispr arrays/product/ATCC
    Average 95 stars, based on 283 article reviews
    distinct crispr arrays - by Bioz Stars, 2026-05
    95/100 stars

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    1) Product Images from "A CRISPR array orchestrates virulence and host response in Porphyromonas gingivalis"

    Article Title: A CRISPR array orchestrates virulence and host response in Porphyromonas gingivalis

    Journal: Microbiology Spectrum

    doi: 10.1128/spectrum.02834-25

    Impact of CRISPR array 30.1 deletion on growth, biofilm formation, and virulence of P. gingivalis ATCC 33277. ( a ) Growth curve comparing planktonic growth of wild-type and ΔCRISPR array 30.1 mutant strains. ( b ) Biofilm biomass quantification of wild-type and ΔCRISPR array 30.1 mutant strains grown on microtiter plates, assessed by safranin staining (OD at 492 nm). ( c–e ) Kaplan–Meier survival analysis of Galleria mellonella larvae injected with different concentrations of wild-type or ΔCRISPR array 30.1 mutant strains: ( c ) 6 × 10 7 CFU/mL; ( d ) 3 × 10 8 CFU/mL; and ( e ) 6 × 10 8 CFU/mL. Survival differences between groups were statistically significant ( P < 0.0001). Controls represent larvae injected with PBS only.
    Figure Legend Snippet: Impact of CRISPR array 30.1 deletion on growth, biofilm formation, and virulence of P. gingivalis ATCC 33277. ( a ) Growth curve comparing planktonic growth of wild-type and ΔCRISPR array 30.1 mutant strains. ( b ) Biofilm biomass quantification of wild-type and ΔCRISPR array 30.1 mutant strains grown on microtiter plates, assessed by safranin staining (OD at 492 nm). ( c–e ) Kaplan–Meier survival analysis of Galleria mellonella larvae injected with different concentrations of wild-type or ΔCRISPR array 30.1 mutant strains: ( c ) 6 × 10 7 CFU/mL; ( d ) 3 × 10 8 CFU/mL; and ( e ) 6 × 10 8 CFU/mL. Survival differences between groups were statistically significant ( P < 0.0001). Controls represent larvae injected with PBS only.

    Techniques Used: CRISPR, Mutagenesis, Staining, Injection

    Deletion of the CRISPR array 30.1 alters cytokine and chemokine secretion by THP-1 macrophages upon P. gingivalis infection. THP-1 cells were infected with wild-type or ΔCRISPR 30.1 P . gingivalis (multiplicity of infection = 100), and supernatants were collected at 2 h and 6 h post-infection. Cytokine and chemokine levels were measured by Luminex multiplex assay. Data are mean ± SD of three independent experiments ( n = 3). Statistical differences were evaluated using a false discovery rate (FDR) value of <0.05 for multiple-comparison corrections comparisons test: * 0.01 < P ≤ .05, ** 0.001 < P ≤ .01, *** P ≤ 0.001 (see Jupyter notebook for details).
    Figure Legend Snippet: Deletion of the CRISPR array 30.1 alters cytokine and chemokine secretion by THP-1 macrophages upon P. gingivalis infection. THP-1 cells were infected with wild-type or ΔCRISPR 30.1 P . gingivalis (multiplicity of infection = 100), and supernatants were collected at 2 h and 6 h post-infection. Cytokine and chemokine levels were measured by Luminex multiplex assay. Data are mean ± SD of three independent experiments ( n = 3). Statistical differences were evaluated using a false discovery rate (FDR) value of <0.05 for multiple-comparison corrections comparisons test: * 0.01 < P ≤ .05, ** 0.001 < P ≤ .01, *** P ≤ 0.001 (see Jupyter notebook for details).

    Techniques Used: CRISPR, Infection, Luminex, Multiplex Assay, Comparison

    PathfindR-derived KEGG pathway enrichment in P. gingivalis and THP-1 cells following infection with the ΔCRISPR 30.1 mutant. Bubble plots display enriched pathways clustered by functional category. The x-axis shows fold enrichment, the y-axis lists KEGG pathway names, bubble size reflects the number of differentially expressed genes (DEGs) in each pathway, and bubble color indicates statistical significance (–log₁₀ of the lowest P -value; deeper red denotes more substantial enrichment). Red pathway labels denote clusters in which all constituent genes are upregulated in the ΔCRISPR 30.1 mutant compared to wild type. ( a ) KEGG pathway enrichment in P. gingivalis at 2 h post-infection. ( b ) KEGG pathway enrichment in P. gingivalis at 6 h post-infection. ( c ) KEGG pathway enrichment in THP-1 cells at 2 h post-infection. ( d ) KEGG pathway enrichment in THP-1 cells at 6 h post-infection.
    Figure Legend Snippet: PathfindR-derived KEGG pathway enrichment in P. gingivalis and THP-1 cells following infection with the ΔCRISPR 30.1 mutant. Bubble plots display enriched pathways clustered by functional category. The x-axis shows fold enrichment, the y-axis lists KEGG pathway names, bubble size reflects the number of differentially expressed genes (DEGs) in each pathway, and bubble color indicates statistical significance (–log₁₀ of the lowest P -value; deeper red denotes more substantial enrichment). Red pathway labels denote clusters in which all constituent genes are upregulated in the ΔCRISPR 30.1 mutant compared to wild type. ( a ) KEGG pathway enrichment in P. gingivalis at 2 h post-infection. ( b ) KEGG pathway enrichment in P. gingivalis at 6 h post-infection. ( c ) KEGG pathway enrichment in THP-1 cells at 2 h post-infection. ( d ) KEGG pathway enrichment in THP-1 cells at 6 h post-infection.

    Techniques Used: Derivative Assay, Infection, Mutagenesis, Functional Assay

    Single-primer amplification (SPA) mapping and PathfindR enrichment. ( a ) SPA positive control: PCR amplification using a mixture of all CRISPR array 30.1 spacers as primers against wild-type genomic DNA yields a single, dominant amplicon corresponding to the CRISPR array itself, confirming the specificity of the primers. ( b ) Genome-wide SPA peak distribution: Mapped SPA amplicon counts across the P. gingivalis chromosome reveal discrete binding sites (peaks) in both coding and intergenic regions, indicating self-targeting by array 30.1 spacers. ( c ) KEGG enrichment, % genes per term: PathfindR analysis of SPA-identified gene targets displays enriched KEGG pathways, plotted as the percentage of total differentially targeted genes annotated to each pathway. Bubble size corresponds to –log₁₀( P -value). ( d ) KEGG enrichment, % terms per cluster: The same enrichment results, grouped by functional clusters, are plotted as the percentage of enriched pathways within each cluster. Bubble size indicates the number of pathways in that cluster, and color intensity reflects statistical significance (–log₁₀( P -value)).
    Figure Legend Snippet: Single-primer amplification (SPA) mapping and PathfindR enrichment. ( a ) SPA positive control: PCR amplification using a mixture of all CRISPR array 30.1 spacers as primers against wild-type genomic DNA yields a single, dominant amplicon corresponding to the CRISPR array itself, confirming the specificity of the primers. ( b ) Genome-wide SPA peak distribution: Mapped SPA amplicon counts across the P. gingivalis chromosome reveal discrete binding sites (peaks) in both coding and intergenic regions, indicating self-targeting by array 30.1 spacers. ( c ) KEGG enrichment, % genes per term: PathfindR analysis of SPA-identified gene targets displays enriched KEGG pathways, plotted as the percentage of total differentially targeted genes annotated to each pathway. Bubble size corresponds to –log₁₀( P -value). ( d ) KEGG enrichment, % terms per cluster: The same enrichment results, grouped by functional clusters, are plotted as the percentage of enriched pathways within each cluster. Bubble size indicates the number of pathways in that cluster, and color intensity reflects statistical significance (–log₁₀( P -value)).

    Techniques Used: Amplification, Positive Control, CRISPR, Genome Wide, Binding Assay, Functional Assay



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    ATCC distinct crispr arrays
    Impact of <t>CRISPR</t> array 30.1 deletion on growth, biofilm formation, and virulence of <t>P.</t> <t>gingivalis</t> ATCC 33277. ( a ) Growth curve comparing planktonic growth of wild-type and ΔCRISPR array 30.1 mutant strains. ( b ) Biofilm biomass quantification of wild-type and ΔCRISPR array 30.1 mutant strains grown on microtiter plates, assessed by safranin staining (OD at 492 nm). ( c–e ) Kaplan–Meier survival analysis of Galleria mellonella larvae injected with different concentrations of wild-type or ΔCRISPR array 30.1 mutant strains: ( c ) 6 × 10 7 CFU/mL; ( d ) 3 × 10 8 CFU/mL; and ( e ) 6 × 10 8 CFU/mL. Survival differences between groups were statistically significant ( P < 0.0001). Controls represent larvae injected with PBS only.
    Distinct Crispr Arrays, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/distinct crispr arrays/product/ATCC
    Average 95 stars, based on 1 article reviews
    distinct crispr arrays - by Bioz Stars, 2026-05
    95/100 stars
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    Impact of CRISPR array 30.1 deletion on growth, biofilm formation, and virulence of P. gingivalis ATCC 33277. ( a ) Growth curve comparing planktonic growth of wild-type and ΔCRISPR array 30.1 mutant strains. ( b ) Biofilm biomass quantification of wild-type and ΔCRISPR array 30.1 mutant strains grown on microtiter plates, assessed by safranin staining (OD at 492 nm). ( c–e ) Kaplan–Meier survival analysis of Galleria mellonella larvae injected with different concentrations of wild-type or ΔCRISPR array 30.1 mutant strains: ( c ) 6 × 10 7 CFU/mL; ( d ) 3 × 10 8 CFU/mL; and ( e ) 6 × 10 8 CFU/mL. Survival differences between groups were statistically significant ( P < 0.0001). Controls represent larvae injected with PBS only.

    Journal: Microbiology Spectrum

    Article Title: A CRISPR array orchestrates virulence and host response in Porphyromonas gingivalis

    doi: 10.1128/spectrum.02834-25

    Figure Lengend Snippet: Impact of CRISPR array 30.1 deletion on growth, biofilm formation, and virulence of P. gingivalis ATCC 33277. ( a ) Growth curve comparing planktonic growth of wild-type and ΔCRISPR array 30.1 mutant strains. ( b ) Biofilm biomass quantification of wild-type and ΔCRISPR array 30.1 mutant strains grown on microtiter plates, assessed by safranin staining (OD at 492 nm). ( c–e ) Kaplan–Meier survival analysis of Galleria mellonella larvae injected with different concentrations of wild-type or ΔCRISPR array 30.1 mutant strains: ( c ) 6 × 10 7 CFU/mL; ( d ) 3 × 10 8 CFU/mL; and ( e ) 6 × 10 8 CFU/mL. Survival differences between groups were statistically significant ( P < 0.0001). Controls represent larvae injected with PBS only.

    Article Snippet: Specifically, P. gingivalis strain ATCC 33277 harbors four distinct CRISPR arrays (30.1, 36.1, 36.2, and 37) linked to type I-B, III, VI-B1, and VI-B2 Cas operons, respectively ( , ).

    Techniques: CRISPR, Mutagenesis, Staining, Injection

    Deletion of the CRISPR array 30.1 alters cytokine and chemokine secretion by THP-1 macrophages upon P. gingivalis infection. THP-1 cells were infected with wild-type or ΔCRISPR 30.1 P . gingivalis (multiplicity of infection = 100), and supernatants were collected at 2 h and 6 h post-infection. Cytokine and chemokine levels were measured by Luminex multiplex assay. Data are mean ± SD of three independent experiments ( n = 3). Statistical differences were evaluated using a false discovery rate (FDR) value of <0.05 for multiple-comparison corrections comparisons test: * 0.01 < P ≤ .05, ** 0.001 < P ≤ .01, *** P ≤ 0.001 (see Jupyter notebook for details).

    Journal: Microbiology Spectrum

    Article Title: A CRISPR array orchestrates virulence and host response in Porphyromonas gingivalis

    doi: 10.1128/spectrum.02834-25

    Figure Lengend Snippet: Deletion of the CRISPR array 30.1 alters cytokine and chemokine secretion by THP-1 macrophages upon P. gingivalis infection. THP-1 cells were infected with wild-type or ΔCRISPR 30.1 P . gingivalis (multiplicity of infection = 100), and supernatants were collected at 2 h and 6 h post-infection. Cytokine and chemokine levels were measured by Luminex multiplex assay. Data are mean ± SD of three independent experiments ( n = 3). Statistical differences were evaluated using a false discovery rate (FDR) value of <0.05 for multiple-comparison corrections comparisons test: * 0.01 < P ≤ .05, ** 0.001 < P ≤ .01, *** P ≤ 0.001 (see Jupyter notebook for details).

    Article Snippet: Specifically, P. gingivalis strain ATCC 33277 harbors four distinct CRISPR arrays (30.1, 36.1, 36.2, and 37) linked to type I-B, III, VI-B1, and VI-B2 Cas operons, respectively ( , ).

    Techniques: CRISPR, Infection, Luminex, Multiplex Assay, Comparison

    PathfindR-derived KEGG pathway enrichment in P. gingivalis and THP-1 cells following infection with the ΔCRISPR 30.1 mutant. Bubble plots display enriched pathways clustered by functional category. The x-axis shows fold enrichment, the y-axis lists KEGG pathway names, bubble size reflects the number of differentially expressed genes (DEGs) in each pathway, and bubble color indicates statistical significance (–log₁₀ of the lowest P -value; deeper red denotes more substantial enrichment). Red pathway labels denote clusters in which all constituent genes are upregulated in the ΔCRISPR 30.1 mutant compared to wild type. ( a ) KEGG pathway enrichment in P. gingivalis at 2 h post-infection. ( b ) KEGG pathway enrichment in P. gingivalis at 6 h post-infection. ( c ) KEGG pathway enrichment in THP-1 cells at 2 h post-infection. ( d ) KEGG pathway enrichment in THP-1 cells at 6 h post-infection.

    Journal: Microbiology Spectrum

    Article Title: A CRISPR array orchestrates virulence and host response in Porphyromonas gingivalis

    doi: 10.1128/spectrum.02834-25

    Figure Lengend Snippet: PathfindR-derived KEGG pathway enrichment in P. gingivalis and THP-1 cells following infection with the ΔCRISPR 30.1 mutant. Bubble plots display enriched pathways clustered by functional category. The x-axis shows fold enrichment, the y-axis lists KEGG pathway names, bubble size reflects the number of differentially expressed genes (DEGs) in each pathway, and bubble color indicates statistical significance (–log₁₀ of the lowest P -value; deeper red denotes more substantial enrichment). Red pathway labels denote clusters in which all constituent genes are upregulated in the ΔCRISPR 30.1 mutant compared to wild type. ( a ) KEGG pathway enrichment in P. gingivalis at 2 h post-infection. ( b ) KEGG pathway enrichment in P. gingivalis at 6 h post-infection. ( c ) KEGG pathway enrichment in THP-1 cells at 2 h post-infection. ( d ) KEGG pathway enrichment in THP-1 cells at 6 h post-infection.

    Article Snippet: Specifically, P. gingivalis strain ATCC 33277 harbors four distinct CRISPR arrays (30.1, 36.1, 36.2, and 37) linked to type I-B, III, VI-B1, and VI-B2 Cas operons, respectively ( , ).

    Techniques: Derivative Assay, Infection, Mutagenesis, Functional Assay

    Single-primer amplification (SPA) mapping and PathfindR enrichment. ( a ) SPA positive control: PCR amplification using a mixture of all CRISPR array 30.1 spacers as primers against wild-type genomic DNA yields a single, dominant amplicon corresponding to the CRISPR array itself, confirming the specificity of the primers. ( b ) Genome-wide SPA peak distribution: Mapped SPA amplicon counts across the P. gingivalis chromosome reveal discrete binding sites (peaks) in both coding and intergenic regions, indicating self-targeting by array 30.1 spacers. ( c ) KEGG enrichment, % genes per term: PathfindR analysis of SPA-identified gene targets displays enriched KEGG pathways, plotted as the percentage of total differentially targeted genes annotated to each pathway. Bubble size corresponds to –log₁₀( P -value). ( d ) KEGG enrichment, % terms per cluster: The same enrichment results, grouped by functional clusters, are plotted as the percentage of enriched pathways within each cluster. Bubble size indicates the number of pathways in that cluster, and color intensity reflects statistical significance (–log₁₀( P -value)).

    Journal: Microbiology Spectrum

    Article Title: A CRISPR array orchestrates virulence and host response in Porphyromonas gingivalis

    doi: 10.1128/spectrum.02834-25

    Figure Lengend Snippet: Single-primer amplification (SPA) mapping and PathfindR enrichment. ( a ) SPA positive control: PCR amplification using a mixture of all CRISPR array 30.1 spacers as primers against wild-type genomic DNA yields a single, dominant amplicon corresponding to the CRISPR array itself, confirming the specificity of the primers. ( b ) Genome-wide SPA peak distribution: Mapped SPA amplicon counts across the P. gingivalis chromosome reveal discrete binding sites (peaks) in both coding and intergenic regions, indicating self-targeting by array 30.1 spacers. ( c ) KEGG enrichment, % genes per term: PathfindR analysis of SPA-identified gene targets displays enriched KEGG pathways, plotted as the percentage of total differentially targeted genes annotated to each pathway. Bubble size corresponds to –log₁₀( P -value). ( d ) KEGG enrichment, % terms per cluster: The same enrichment results, grouped by functional clusters, are plotted as the percentage of enriched pathways within each cluster. Bubble size indicates the number of pathways in that cluster, and color intensity reflects statistical significance (–log₁₀( P -value)).

    Article Snippet: Specifically, P. gingivalis strain ATCC 33277 harbors four distinct CRISPR arrays (30.1, 36.1, 36.2, and 37) linked to type I-B, III, VI-B1, and VI-B2 Cas operons, respectively ( , ).

    Techniques: Amplification, Positive Control, CRISPR, Genome Wide, Binding Assay, Functional Assay