histone modification chip-seq data  (Broad Institute Inc)

Journal: Nature Communications

Article Title: EPOP restricts PRC2.1 targeting to chromatin by directly modulating enzyme complex dimerization

doi: 10.1038/s41467-025-68280-5

Figure Lengend Snippet: a Re-expression of WT and mutant EPOP in mESCs. Representative of two biological replicates . b Co-IP assay of re-expressed EPOP. The re-expressed 3 × FLAG-EPOP-HA protein was used as the bait, and the bound endogenous SUZ12 was detected. Representative of two replicates. c Schematic of the EpiLC differentiation. Some parts of the figure were created in BioRender. Liu, X. (2026) ( https://biorender.com/gvraoqv ). d Heatmaps of ChIP-seq replicates. Using the FDR < 0.05 threshold, the gain-of-signal MTF2 (purple) and H3K27me3 (green) peaks from individual replicates (WT-1, WT-2, D5-1, and D5-2) are shown in the heatmaps. The centers of the consensus binding sites are aligned. The number of the consensus binding sites is labeled. e Metaplots of ChIP-seq replicates. The mean ChIP-seq signal of the differential MTF2 (upper panel) and H3K27me3 (lower panel) peaks shown in ( d ) is plotted. The individual replicates are color-coded. f Genome browser tracks of selected gene loci. Tracks were generated by SparK ( https://github.com/harbourlab/SparK ). Genomic coordinates are provided. The difference between the replicates, calculated as the standard deviation, is indicated as the shaded areas surrounding the tracks. g Scatter plots of MTF2 and H3K27me3. MTF2 (left panel) and H3K27me3 (right panel) reads were normalized by the total reads. The mean read concentration corresponding to log2 (normalized ChIP-seq reads with input reads subtracted) was calculated by DiffBind.

Article Snippet: For the shRNA KD ChIP-seq data sequenced by Novogene, the raw sequencing reads were trimmed by Cutadapt and then mapped by Bowtie 2 with the “--very-sensitive” parameter.

Techniques: Expressing, Mutagenesis, Co-Immunoprecipitation Assay, ChIP-sequencing, Binding Assay, Labeling, Generated, Standard Deviation, Concentration Assay

Journal: Nature Communications

Article Title: EPOP restricts PRC2.1 targeting to chromatin by directly modulating enzyme complex dimerization

doi: 10.1038/s41467-025-68280-5

Figure Lengend Snippet: a Heatmaps of ChIP-seq replicates. The differential MTF2 peaks between the EPOP WT and EPOP D5 EpiLCs were grouped into three categories based on the response to shRNA KD, using the FDR < 0.05 threshold. Differential peaks shared by the control and Elongin B KD are labeled as n1, differential peaks unique to the control KD are labeled as n2, and differential peaks unique to the Elongin B KD are labeled as n3. b Genome browser tracks of selected gene loci. Tracks were generated by SparK. Two gene loci associated with the shared differential MTF2 peaks between the control KD and the Elongin B KD are shown. c Venn diagram of the differential MTF2 peaks in the three categories.

Article Snippet: For the shRNA KD ChIP-seq data sequenced by Novogene, the raw sequencing reads were trimmed by Cutadapt and then mapped by Bowtie 2 with the “--very-sensitive” parameter.

Techniques: ChIP-sequencing, shRNA, Control, Labeling, Generated

Journal: Nature Communications

Article Title: EPOP restricts PRC2.1 targeting to chromatin by directly modulating enzyme complex dimerization

doi: 10.1038/s41467-025-68280-5

Figure Lengend Snippet: a Volcano plot of differential gene expression. RNA-seq results of the EPOP D5 EpiLCs in triplicates were compared to those of the EPOP WT EpiLCs. The number of upregulated and downregulated genes is indicated. Data passing the FDR < 0.05, FC > 1.5, and average TPM of WT or mutant > 0.5 thresholds were analyzed. b Correlation of RNA-seq and ChIP-seq. One ChIP-seq replicate is shown here, and the other replicate is shown in the supplemental materials. The differential gene expression was aligned with the differential MTF2 enrichment around the transcription start site (TSS). The corresponding H3K27me3 signals are also displayed. Compared to the WT counterpart, 130 genes in the EPOP D5 EpiLCs were downregulated and associated with enhanced MTF2 signals around the TSS. The other 318 downregulated genes were not associated with EPOP-regulated MTF2 targeting. 187 upregulated genes are shown as well. c Gene ontology analysis. The PRC2.1-repressed, EPOP-maintained genes were subjected to gene ontology analysis on the DAVID server. The top 5 overrepresented terms in molecular function are shown. The p -value is one-tail Fisher Exact probability value used for gene-enrichment analysis by the DAVID server. d Schematic model of developmental gene repression by PRC2. On the left, the transient intrinsic dimer of the PRC2 core complex is illustrated. In the middle, distinct oligomerization states of various PRC2.1 and PRC2.2 holocomplexes are highlighted. MTF2 mediates direct chromatin binding, and it also stabilizes the intrinsic dimer, promoting chromatin targeting of the dimeric PRC2.1, likely via an avidity effect. EPOP disrupts the dimeric architecture of PRC2.1, containing MTF2, restricts PRC2.1 targeting, and thereby maintains the limited expression of PRC2.1-repressed developmental regulators. On the right, the PRC2.1-dependent role of EPOP in early development is illustrated. Black solid curve: during the ESC differentiation, a set of key gene regulators is repressed by PRC2.1, with limited expression being maintained by the EPOP-mediated inhibition of PRC2.1 targeting, which is followed by upregulation of the same set of gene regulators, leading to cell fate 1, e.g., PGCLCs. Gray dotted curve: the absence of EPOP results in the over-repression of these gene regulators by PRC2.1, which may change stem cell differentiation trajectories and result in an alternative cell fate 2. Some parts of the figure were created in BioRender. Liu, X. (2026) ( https://biorender.com/l3ji249 ).

Article Snippet: For the shRNA KD ChIP-seq data sequenced by Novogene, the raw sequencing reads were trimmed by Cutadapt and then mapped by Bowtie 2 with the “--very-sensitive” parameter.

Techniques: Gene Expression, RNA Sequencing, Mutagenesis, ChIP-sequencing, Binding Assay, Expressing, Inhibition, Cell Differentiation

Journal: The Journal of Biological Chemistry

Article Title: HMGN1 and HMGN2 are recruited to acetylated and histone variant H2A.Z-containing nucleosomes to regulate chromatin state and transcription

doi: 10.1016/j.jbc.2025.110997

Figure Lengend Snippet: HMGN proteins localize to transcriptionally active regions of the genome . A , genome browser tracks of HMGN1, HMGN2, H3K27ac, H3K4me3, H2A.Z, RAD21, and CTCF ChIP-Seq signal at the promoter of Sox2 and the super-enhancer domain downstream of Sox2 in WT mESCs. B , Pearson’s correlation hierarchical clustering heatmap of genome-wide signal of HMGN1, HMGN2, H3K27ac, H3K4me3, H2A.Z, RAD21, and CTCF ChIP-Seq datasets in WT mESCs. C , bar graph of the number of expressed genes and non-expressed genes in the mouse embryonic stem cell (mESC) genome bound and not bound by HMGN1 and HMGN2. Active genes are defined as genes with a RPKM value ≥22 as defined by the EMBL Expression Atlas. D , UpSet plot of HMGN1 ChIP-Seq peaks in WT mESCs displaying intersection of sets of peaks at H3K27ac, H3K4me3, transcription start sites (TSSs), H2A.Z, RAD21, CTCF, and other sites. E , bar graph of the number of HMGN1 peaks that overlap with H3K4me3, H3K27ac, CTCF, H2A.Z, TSSs, RAD21, and other peaks in WT mESCs. F , average signal plot of HMGN1, HMGN2, H3K27ac, H3K4me3, H2A.Z, RAD21, and CTCF ChIP-Seq signal at a union list of all HMGN1 and HMGN2 peaks (Z-score normalized). G , clustered heatmaps of HMGN1, HMGN2, H3K27ac, H3K4me3, H2A.Z, RAD21, and CTCF ChIP-Seq signal at active enhancers, active promoters, and insulator sites, ordered by HMGN2 signal (Z-score normalized). H , average signal plots of HMGN1, HMGN2, H3K27ac, H3K4me3, H2A.Z, RAD21, and CTCF ChIP-Seq signal in WT mESCs at active enhancers, active promoters, and insulator sites (Z-score normalized). ChIP-Seq, chromatin immunoprecipitation followed by sequencing; HMGN, High Mobility Nucleosome-binding protein; mESC, mouse embryonic stem cell; RPKM, reads per kilobase of transcript per million mapped reads.

Article Snippet: Previously collected and reported ChIP-Seq data used in this study are summarized in and can also be found in the National Center for Biotechnology Information Gene Expression Omnibus repository.

Techniques: ChIP-sequencing, Genome Wide, Expressing, Chromatin Immunoprecipitation, Sequencing, Binding Assay

Journal: The Journal of Biological Chemistry

Article Title: HMGN1 and HMGN2 are recruited to acetylated and histone variant H2A.Z-containing nucleosomes to regulate chromatin state and transcription

doi: 10.1016/j.jbc.2025.110997

Figure Lengend Snippet: Cohesin and CTCF localization on chromatin is not dependent on HMGN1 or HMGN2 . A , genome browser tracks of RAD21 and CTCF ChIP-Seq signal near the promoter of Zbp1 (differentially expressed gene in Hmgn1 −/− Hmgn2 −/− mESCs) in WT mESCs and Hmgn1 −/− Hmgn2 −/− mESCs. B , MA plot showing differential enrichment of RAD21 signal between WT mESCs and Hmgn1 −/− Hmgn2 −/− mESCs at conserved binding sites. C , MA plot showing differential enrichment of CTCF signal between WT mESCs and Hmgn1 −/− Hmgn2 −/− mESCs at conserved binding sites. D , average signal plots of RAD21 and CTCF ChIP-Seq signal at a union list of all HMGN1 and HMGN2 peaks in WT mESCs and Hmgn1 −/− Hmgn2 −/− mESCs (Z-score normalized). E , average signal plots of RAD21 and CTCF ChIP-Seq signal in WT mESCs and Hmgn1 −/− Hmgn2 −/− mESCs at CTCF sites, cohesin sites, active enhancers, and transcription start sites (TSSs). F , ChIP-Seq signal of RAD21 and CTCF in WT mESCs and Hmgn1 −/− Hmgn2 −/− mESCs shown at the promoters of upregulated and downregulated differently expressed genes in either Hmgn1 −/− mESCs, Hmgn2 −/− mESCs, or Hmgn1 −/− Hmgn2 −/− mESCs. ChIP-Seq, chromatin immunoprecipitation followed by sequencing; HMGN, High Mobility Nucleosome-binding protein; mESC, mouse embryonic stem cell.

Article Snippet: Previously collected and reported ChIP-Seq data used in this study are summarized in and can also be found in the National Center for Biotechnology Information Gene Expression Omnibus repository.

Techniques: ChIP-sequencing, Binding Assay, Chromatin Immunoprecipitation, Sequencing

Journal: Bioinformatics

Article Title: Chrom-Sig: de-noising 1D genomic profiles by signal processing methods

doi: 10.1093/bioinformatics/btaf645

Figure Lengend Snippet: Chrom-Sig results on GM12878 CTCF ChIP-seq and CUT&RUN datasets. (a) Browser views of CTCF binding motifs with orientation (blue triangles) and coverage tracks generated by piling up the original (before Chrom-Sig) and Chrom-Sig ‘pass’ or ‘fail’ reads, accompanied by the peaks called by SICER. (b) Venn diagram of the peaks called on the original and Chrom-Sig ‘pass’ reads pile-up reads using false discovery rate (FDR) of 0.1 and 5000 pseudo-reads, with boxplots of maximum peak intensity for each peak. (c) Number of peaks overlapping CTCF motifs, and top MEME result on the original GM12878 CTCF CUT&RUN data before Chrom-Sig. (d) Similar to panel c for Chrom-Sig ‘pass’ results.

Article Snippet: For example, the GM12878 CTCF ChIP-seq data were originally noisy with a large portion of reads in non-binding sites, but Chrom-Sig with FDR of 0.1 retained only the reads with strong binding ( ).

Techniques: ChIP-sequencing, Binding Assay, Generated