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dimethylsulfoxid (dmso) solvent control  (Carl Roth GmbH)

 
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    Carl Roth GmbH dimethylsulfoxid (dmso) solvent control
    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
    Dimethylsulfoxid (Dmso) Solvent Control, supplied by Carl Roth GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/control+solvent/dimethylsulfoxid++dmso++solvent+control/pmc12143595-33-4-9
    Average 90 stars, based on 1 article reviews
    dimethylsulfoxid (dmso) solvent control - by Bioz Stars, 2026-10
    90/100 stars

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    1) Product Images from "p53 reveals principles of chromatin remodeling and enhancer activation"

    Article Title: p53 reveals principles of chromatin remodeling and enhancer activation

    Journal: Nucleic Acids Research

    doi: 10.1093/nar/gkaf465

    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
    Figure Legend Snippet: p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.

    Techniques Used: Control, Binding Assay, ChIP-sequencing

    p53 establishes enhancers. ( A ) p53 binding sites were sorted by local chromatin state (promoter, enhancer, transcription, quiescent). In addition, they were sorted by the presence (open) or absence (closed) of an ATAC-seq peak in Nutlin-3a and DMSO control conditions. ( B ) CUT&Tag for H3K4me1 and H3K27ac was performed on two biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. H3K4me1, H3K27ac, ATAC-seq, and p53 ChIP-seq signals are displayed for p53 binding sites that were closed in the DMSO control condition and open ( C ) or closed ( D ) in the Nutlin-3a treatment condition. Regions were sorted by average signal and p53 binding sites located in promoters were removed for visualization purposes because of the small group size and different signal scales. ( E ) p53 occupancy (CPM) at p53 binding sites in the different groups. Significance determined using a two-tailed Kruskal–Wallis test. *** P -value <.001.
    Figure Legend Snippet: p53 establishes enhancers. ( A ) p53 binding sites were sorted by local chromatin state (promoter, enhancer, transcription, quiescent). In addition, they were sorted by the presence (open) or absence (closed) of an ATAC-seq peak in Nutlin-3a and DMSO control conditions. ( B ) CUT&Tag for H3K4me1 and H3K27ac was performed on two biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. H3K4me1, H3K27ac, ATAC-seq, and p53 ChIP-seq signals are displayed for p53 binding sites that were closed in the DMSO control condition and open ( C ) or closed ( D ) in the Nutlin-3a treatment condition. Regions were sorted by average signal and p53 binding sites located in promoters were removed for visualization purposes because of the small group size and different signal scales. ( E ) p53 occupancy (CPM) at p53 binding sites in the different groups. Significance determined using a two-tailed Kruskal–Wallis test. *** P -value <.001.

    Techniques Used: Binding Assay, Control, ChIP-sequencing, Two Tailed Test

    p53-induced transcription correlates with chromatin remodeling and requires high p53 abundance. ( A ) CAGE-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Significantly differentially regulated TSSs were identified. ( B ) Enrichment of transcription factor binding sites at sites with increased (left) or decreased (right) TSS activity upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) Comparison of changes in TSS activity (CAGE-seq) and DNA accessibility (ATAC-seq) for all TSSs in accessible DNA regions (determined by ATAC-seq peaks) upon Nutlin-3a treatment. ( D ) Subsets of TSSs/accessible sites that overlap with p53 (top panel), E2F4 (middle panel), and RFX7 binding sites (bottom panel). ( E ) p53 ChIP-seq, ATAC-seq, H3K4me1, and H3K27ac signals at p53 binding sites located in promoter regions. Subgroups were determined by overlaps with an induced TSS (log 2 FC > 0.5), uninduced TSS (log 2 FC < 0.5), and no TSS. Regions sorted by H3K27ac signal. ( F ) Comparison of changes in local transcription (CAGE-seq) and p53 occupancy (CPM from ChIP-seq). Significance determined by two-tailed Spearman correlation. Sigmoidal fit obtained best r 2 . ( G ) The fraction of promoter p53 binding sites with a canonical p53RE, noncanonical p53RE, and no p53RE.
    Figure Legend Snippet: p53-induced transcription correlates with chromatin remodeling and requires high p53 abundance. ( A ) CAGE-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Significantly differentially regulated TSSs were identified. ( B ) Enrichment of transcription factor binding sites at sites with increased (left) or decreased (right) TSS activity upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) Comparison of changes in TSS activity (CAGE-seq) and DNA accessibility (ATAC-seq) for all TSSs in accessible DNA regions (determined by ATAC-seq peaks) upon Nutlin-3a treatment. ( D ) Subsets of TSSs/accessible sites that overlap with p53 (top panel), E2F4 (middle panel), and RFX7 binding sites (bottom panel). ( E ) p53 ChIP-seq, ATAC-seq, H3K4me1, and H3K27ac signals at p53 binding sites located in promoter regions. Subgroups were determined by overlaps with an induced TSS (log 2 FC > 0.5), uninduced TSS (log 2 FC < 0.5), and no TSS. Regions sorted by H3K27ac signal. ( F ) Comparison of changes in local transcription (CAGE-seq) and p53 occupancy (CPM from ChIP-seq). Significance determined by two-tailed Spearman correlation. Sigmoidal fit obtained best r 2 . ( G ) The fraction of promoter p53 binding sites with a canonical p53RE, noncanonical p53RE, and no p53RE.

    Techniques Used: Control, Binding Assay, Activity Assay, Comparison, ChIP-sequencing, Two Tailed Test

    p53 preferentially directs transcription initiation to the p53RE and other sites within 100 bp. ( A ) Positional p53 motif enrichment relative to the CAGE-seq-detected TSS (CTSS) identified by HOMER2. The density of CTSSs at ±200 bp around canonical p53REs of p53 binding sites in ( B ) Nutlin-3a and DMSO control samples and ( C ) the Nutlin-3a data separated by EpiMap-derived chromatin states. ( D ) Genome browser images displaying CAGE-seq data among p53 ChIP-seq, ATAC-seq, and CUT&Tag (H3K4me1 and H3K27ac) data at two p53 binding sites. The predicted p53RE is highlighted. p53 ChIP-seq, nucleosome-free ATAC-seq, and CUT&Tag data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS. CTSSs were coverage normalized. ( E ) Dynamic p53 binding is required for Pol II initiation after its recruitment to the edges of nucleosome-depleted regions.
    Figure Legend Snippet: p53 preferentially directs transcription initiation to the p53RE and other sites within 100 bp. ( A ) Positional p53 motif enrichment relative to the CAGE-seq-detected TSS (CTSS) identified by HOMER2. The density of CTSSs at ±200 bp around canonical p53REs of p53 binding sites in ( B ) Nutlin-3a and DMSO control samples and ( C ) the Nutlin-3a data separated by EpiMap-derived chromatin states. ( D ) Genome browser images displaying CAGE-seq data among p53 ChIP-seq, ATAC-seq, and CUT&Tag (H3K4me1 and H3K27ac) data at two p53 binding sites. The predicted p53RE is highlighted. p53 ChIP-seq, nucleosome-free ATAC-seq, and CUT&Tag data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS. CTSSs were coverage normalized. ( E ) Dynamic p53 binding is required for Pol II initiation after its recruitment to the edges of nucleosome-depleted regions.

    Techniques Used: Binding Assay, Control, Derivative Assay, ChIP-sequencing

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    Real-time Polymerase Chain Reaction:

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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
    Dimethylsulfoxid (Dmso) Solvent Control, supplied by Carl Roth GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
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    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and <t>DMSO</t> control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.
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    Image Search Results


    circTACC3 m 6 A modification is associated with its intracellular localization. (A) Representative image of H&E staining of MASH‐related HCC tumor and paired peritumoral normal tissue derived organoids with relatively low (#1) and high (#2) circTACC3 expression, treated with or without PA + OA. (B) 3D fluorescence scanning of 3‐OH BrDU probe (green), anti‐Ki‐67 antibody (magenta), and DAPI (blue) indicated tissue derived organoids, treated with or without PA + OA; maximum projection of signals is shown. (C‐D) Assays of fluorescence staining with the 3‐OH BrDU probe were conducted on the cell lines with different nuclear circTACC3 level (C, n = 6) and circTACC3 knockout cell strains or negative controls (D, n = 9). The numbers on the Y‐axis represent the apoptotic rate normalized to baseline of 1. ** P < 0.01; *** P < 0.001; NS , not significant. (E) MeRIP assay shows an enrichment of m 6 A‐modified circTACC3 in cytoplasmic and nuclear fraction of HCCLM3 cells. (F) Representation of predicted m 6 A modification motif of circTACC3 (predicted using the SRAMP website). (G) Absolute quantitative RT‐qPCR of m 6 A RNA shows m 6 A modification ratio of intra‐nuclear circTACC3 in the individual motif scale. (H) The m 6 A modification levels of circTACC3 were evaluated by MeRIP in m 6 A inhibitor treated group compared to control (DMSO) group, and in PA + OA treated group compared to control (Mock) group, respectively ( n = 3). *** P < 0.001. (I) Nucleo‐plasmic fractionation to evaluate circTACC3 expression after indicated treatment ( n = 4). *** P < 0.001. (J) 3D‐FISH conducted on MASH‐related HCC tumor tissue derived organoids demonstrates the 3D distribution of circTACC3 (red) in nuclei (blue). (K) H&E staining of MASH‐related HCC tumor tissue derived organoids treated with PA + OA and/or m 6 A intervention. Abbreviations: PA, palmitic acid; OA, oleic acid; T, tumor tissues; PT, peritumoral normal tissue; H&E, hematoxylin and eosin; MeRIP, methylated RNA immunoprecipitation; m 6 A, N6‐methyladenosine; NAS, Non‐alcoholic fatty liver disease activity score; SAH, S‐adenosylhomocysteine; DAA, 3‐deazaadenosine; FISH, fluorescence i n situ hybridization.

    Journal: Cancer Communications

    Article Title: Intranuclear paraspeckle‐circular RNA TACC3 assembly forms RNA‐DNA hybrids to facilitate MASH‐related hepatocellular carcinoma growth in an m 6 A‐dependent manner

    doi: 10.1002/cac2.70061

    Figure Lengend Snippet: circTACC3 m 6 A modification is associated with its intracellular localization. (A) Representative image of H&E staining of MASH‐related HCC tumor and paired peritumoral normal tissue derived organoids with relatively low (#1) and high (#2) circTACC3 expression, treated with or without PA + OA. (B) 3D fluorescence scanning of 3‐OH BrDU probe (green), anti‐Ki‐67 antibody (magenta), and DAPI (blue) indicated tissue derived organoids, treated with or without PA + OA; maximum projection of signals is shown. (C‐D) Assays of fluorescence staining with the 3‐OH BrDU probe were conducted on the cell lines with different nuclear circTACC3 level (C, n = 6) and circTACC3 knockout cell strains or negative controls (D, n = 9). The numbers on the Y‐axis represent the apoptotic rate normalized to baseline of 1. ** P < 0.01; *** P < 0.001; NS , not significant. (E) MeRIP assay shows an enrichment of m 6 A‐modified circTACC3 in cytoplasmic and nuclear fraction of HCCLM3 cells. (F) Representation of predicted m 6 A modification motif of circTACC3 (predicted using the SRAMP website). (G) Absolute quantitative RT‐qPCR of m 6 A RNA shows m 6 A modification ratio of intra‐nuclear circTACC3 in the individual motif scale. (H) The m 6 A modification levels of circTACC3 were evaluated by MeRIP in m 6 A inhibitor treated group compared to control (DMSO) group, and in PA + OA treated group compared to control (Mock) group, respectively ( n = 3). *** P < 0.001. (I) Nucleo‐plasmic fractionation to evaluate circTACC3 expression after indicated treatment ( n = 4). *** P < 0.001. (J) 3D‐FISH conducted on MASH‐related HCC tumor tissue derived organoids demonstrates the 3D distribution of circTACC3 (red) in nuclei (blue). (K) H&E staining of MASH‐related HCC tumor tissue derived organoids treated with PA + OA and/or m 6 A intervention. Abbreviations: PA, palmitic acid; OA, oleic acid; T, tumor tissues; PT, peritumoral normal tissue; H&E, hematoxylin and eosin; MeRIP, methylated RNA immunoprecipitation; m 6 A, N6‐methyladenosine; NAS, Non‐alcoholic fatty liver disease activity score; SAH, S‐adenosylhomocysteine; DAA, 3‐deazaadenosine; FISH, fluorescence i n situ hybridization.

    Article Snippet: STM2457, S‐adenosylhomocysteine (SAH), 3‐deazaadenosine (DAA) or the solvent control DMSO (v/v = 1/1000, #HY‐Y0320, MedChemExpress, NJ, US) was added on Day 4.

    Techniques: Modification, Staining, Derivative Assay, Expressing, Fluorescence, Knock-Out, Quantitative RT-PCR, Control, Fractionation, Methylation, RNA Immunoprecipitation, Activity Assay, Hybridization

    p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.

    Journal: Nucleic Acids Research

    Article Title: p53 reveals principles of chromatin remodeling and enhancer activation

    doi: 10.1093/nar/gkaf465

    Figure Lengend Snippet: p53 is a pioneer factor that increases DNA accessibility. ( A ) ATAC-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Accessible sites were identified by peak calling, and their differential accessibility was assessed. ( B ) Enrichment of transcription factor binding sites that overlap sites with increased (left) or decreased (right) accessibility upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) The presence (open) or absence (closed) of an ATAC-seq peak has been assessed at 7705 recurrent p53 binding sites, and changes between the Nutlin-3a and DMSO control conditions are displayed. ( D ) p53 ChIP-seq and ATAC-seq signals are displayed for the groups identified in panel (C). Regions sorted by ATAC-seq signal. Genome browser images displaying p53 ChIP-seq and ATAC-seq data at a p53 binding site ( E ) that became accessible and ( F ) that remained inaccessible upon Nutlin-3a treatment. The predicted p53RE is highlighted. p53 ChIP-seq and nucleosome-free ATAC-seq data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS according to library size and accessible DNA background.

    Article Snippet: Cells were treated with Dimethylsulfoxid (DMSO) solvent control (0.15%; Carl Roth, Karlsruhe, Germany) or Nutlin-3a (10 μM; MedChemExpress, Monmouth Junction, NJ, USA) for 24 h.

    Techniques: Control, Binding Assay, ChIP-sequencing

    p53 establishes enhancers. ( A ) p53 binding sites were sorted by local chromatin state (promoter, enhancer, transcription, quiescent). In addition, they were sorted by the presence (open) or absence (closed) of an ATAC-seq peak in Nutlin-3a and DMSO control conditions. ( B ) CUT&Tag for H3K4me1 and H3K27ac was performed on two biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. H3K4me1, H3K27ac, ATAC-seq, and p53 ChIP-seq signals are displayed for p53 binding sites that were closed in the DMSO control condition and open ( C ) or closed ( D ) in the Nutlin-3a treatment condition. Regions were sorted by average signal and p53 binding sites located in promoters were removed for visualization purposes because of the small group size and different signal scales. ( E ) p53 occupancy (CPM) at p53 binding sites in the different groups. Significance determined using a two-tailed Kruskal–Wallis test. *** P -value <.001.

    Journal: Nucleic Acids Research

    Article Title: p53 reveals principles of chromatin remodeling and enhancer activation

    doi: 10.1093/nar/gkaf465

    Figure Lengend Snippet: p53 establishes enhancers. ( A ) p53 binding sites were sorted by local chromatin state (promoter, enhancer, transcription, quiescent). In addition, they were sorted by the presence (open) or absence (closed) of an ATAC-seq peak in Nutlin-3a and DMSO control conditions. ( B ) CUT&Tag for H3K4me1 and H3K27ac was performed on two biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. H3K4me1, H3K27ac, ATAC-seq, and p53 ChIP-seq signals are displayed for p53 binding sites that were closed in the DMSO control condition and open ( C ) or closed ( D ) in the Nutlin-3a treatment condition. Regions were sorted by average signal and p53 binding sites located in promoters were removed for visualization purposes because of the small group size and different signal scales. ( E ) p53 occupancy (CPM) at p53 binding sites in the different groups. Significance determined using a two-tailed Kruskal–Wallis test. *** P -value <.001.

    Article Snippet: Cells were treated with Dimethylsulfoxid (DMSO) solvent control (0.15%; Carl Roth, Karlsruhe, Germany) or Nutlin-3a (10 μM; MedChemExpress, Monmouth Junction, NJ, USA) for 24 h.

    Techniques: Binding Assay, Control, ChIP-sequencing, Two Tailed Test

    p53-induced transcription correlates with chromatin remodeling and requires high p53 abundance. ( A ) CAGE-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Significantly differentially regulated TSSs were identified. ( B ) Enrichment of transcription factor binding sites at sites with increased (left) or decreased (right) TSS activity upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) Comparison of changes in TSS activity (CAGE-seq) and DNA accessibility (ATAC-seq) for all TSSs in accessible DNA regions (determined by ATAC-seq peaks) upon Nutlin-3a treatment. ( D ) Subsets of TSSs/accessible sites that overlap with p53 (top panel), E2F4 (middle panel), and RFX7 binding sites (bottom panel). ( E ) p53 ChIP-seq, ATAC-seq, H3K4me1, and H3K27ac signals at p53 binding sites located in promoter regions. Subgroups were determined by overlaps with an induced TSS (log 2 FC > 0.5), uninduced TSS (log 2 FC < 0.5), and no TSS. Regions sorted by H3K27ac signal. ( F ) Comparison of changes in local transcription (CAGE-seq) and p53 occupancy (CPM from ChIP-seq). Significance determined by two-tailed Spearman correlation. Sigmoidal fit obtained best r 2 . ( G ) The fraction of promoter p53 binding sites with a canonical p53RE, noncanonical p53RE, and no p53RE.

    Journal: Nucleic Acids Research

    Article Title: p53 reveals principles of chromatin remodeling and enhancer activation

    doi: 10.1093/nar/gkaf465

    Figure Lengend Snippet: p53-induced transcription correlates with chromatin remodeling and requires high p53 abundance. ( A ) CAGE-seq was performed on four biological replicates of Nutlin-3a and DMSO control-treated MCF-7 cells. Significantly differentially regulated TSSs were identified. ( B ) Enrichment of transcription factor binding sites at sites with increased (left) or decreased (right) TSS activity upon Nutlin-3a treatment. The top 15 transcription factors are displayed. ( C ) Comparison of changes in TSS activity (CAGE-seq) and DNA accessibility (ATAC-seq) for all TSSs in accessible DNA regions (determined by ATAC-seq peaks) upon Nutlin-3a treatment. ( D ) Subsets of TSSs/accessible sites that overlap with p53 (top panel), E2F4 (middle panel), and RFX7 binding sites (bottom panel). ( E ) p53 ChIP-seq, ATAC-seq, H3K4me1, and H3K27ac signals at p53 binding sites located in promoter regions. Subgroups were determined by overlaps with an induced TSS (log 2 FC > 0.5), uninduced TSS (log 2 FC < 0.5), and no TSS. Regions sorted by H3K27ac signal. ( F ) Comparison of changes in local transcription (CAGE-seq) and p53 occupancy (CPM from ChIP-seq). Significance determined by two-tailed Spearman correlation. Sigmoidal fit obtained best r 2 . ( G ) The fraction of promoter p53 binding sites with a canonical p53RE, noncanonical p53RE, and no p53RE.

    Article Snippet: Cells were treated with Dimethylsulfoxid (DMSO) solvent control (0.15%; Carl Roth, Karlsruhe, Germany) or Nutlin-3a (10 μM; MedChemExpress, Monmouth Junction, NJ, USA) for 24 h.

    Techniques: Control, Binding Assay, Activity Assay, Comparison, ChIP-sequencing, Two Tailed Test

    p53 preferentially directs transcription initiation to the p53RE and other sites within 100 bp. ( A ) Positional p53 motif enrichment relative to the CAGE-seq-detected TSS (CTSS) identified by HOMER2. The density of CTSSs at ±200 bp around canonical p53REs of p53 binding sites in ( B ) Nutlin-3a and DMSO control samples and ( C ) the Nutlin-3a data separated by EpiMap-derived chromatin states. ( D ) Genome browser images displaying CAGE-seq data among p53 ChIP-seq, ATAC-seq, and CUT&Tag (H3K4me1 and H3K27ac) data at two p53 binding sites. The predicted p53RE is highlighted. p53 ChIP-seq, nucleosome-free ATAC-seq, and CUT&Tag data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS. CTSSs were coverage normalized. ( E ) Dynamic p53 binding is required for Pol II initiation after its recruitment to the edges of nucleosome-depleted regions.

    Journal: Nucleic Acids Research

    Article Title: p53 reveals principles of chromatin remodeling and enhancer activation

    doi: 10.1093/nar/gkaf465

    Figure Lengend Snippet: p53 preferentially directs transcription initiation to the p53RE and other sites within 100 bp. ( A ) Positional p53 motif enrichment relative to the CAGE-seq-detected TSS (CTSS) identified by HOMER2. The density of CTSSs at ±200 bp around canonical p53REs of p53 binding sites in ( B ) Nutlin-3a and DMSO control samples and ( C ) the Nutlin-3a data separated by EpiMap-derived chromatin states. ( D ) Genome browser images displaying CAGE-seq data among p53 ChIP-seq, ATAC-seq, and CUT&Tag (H3K4me1 and H3K27ac) data at two p53 binding sites. The predicted p53RE is highlighted. p53 ChIP-seq, nucleosome-free ATAC-seq, and CUT&Tag data were normalized to CPM. Mono-nucleosome ATAC-seq data were normalized by DANPOS. CTSSs were coverage normalized. ( E ) Dynamic p53 binding is required for Pol II initiation after its recruitment to the edges of nucleosome-depleted regions.

    Article Snippet: Cells were treated with Dimethylsulfoxid (DMSO) solvent control (0.15%; Carl Roth, Karlsruhe, Germany) or Nutlin-3a (10 μM; MedChemExpress, Monmouth Junction, NJ, USA) for 24 h.

    Techniques: Binding Assay, Control, Derivative Assay, ChIP-sequencing