Acetylation of H3K115 is associated with fragile nucleosomes at CpG island promoters and active regulatory sites
- MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, United Kingdom
- MRC Centre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, United Kingdom
- Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), France
- Division of Cancer Biology, The Institute of Cancer Research, United Kingdom
- Department of Lymphoma, Peking University Cancer Hospital and Institute, Peking University International Cancer Institute, Peking University Health Science Center, China
Figures
Figure 1 with 1 supplement
H3K115ac is associated with CpG island (CGI) promoters.
(A) Nucleosome structure looking down on the dyad axis (modified from PDB-5X7X, Taguchi et al., 2017). The two H3 molecules are shown in cyan and yellow, other histones are in orange and DNA in green. N-terminal histone tails are hidden. Both copies of H3K115 (red and asterisked) are juxtaposed at the dyad axis close to the overlying DNA. (B) Pearson’s correlation matrix with hierarchical clustering in mouse embryonic stem cells (mESCs). Correlation is computed for read counts in 10 kb windows across the genome for ATAC-seq data, ChIP-seq data for active (H3K122ac/H3K27ac/H3K27ac: GSE66023; H3K4me3: GSM1003756; H3K4me1: GSM1003750; and repressive H3K27me3: GSM1276707), histone H3 modifications and for H3K115ac. (C) Proportions of H3K115ac, H3K122ac, and H3K27ac ChIP peaks that overlap genomic segments defined by chromHMM in the mouse genome (Ernst and Kellis, 2012; Pintacuda et al., 2017). (D) Heatmap of H3K115ac ChIP-seq signal (this study), H3K122ac, and H3K27ac (Pradeepa et al., 2016) in mESCs with respect to transcription start site (TSS) of the top 50% of genes by expression and sorted by decreasing gene expression. (E) UCSC genome browser screenshot showing ChIP-seq data for H3K115ac, H3K122ac, H3K27ac, and ATAC-seq in mESCs at the Sox2, Klf4, and Nanog loci. CGIs are indicated. Genome co-ordinates (Mb) are from the mm10 assembly of the mouse genome. (F) Mean normalised reads of, (upper left) 4SU sequencing (4SU-seq) centred at TSS of top 50% genes by expression (4SUseq tags in TSS+ 500 bp region). Genes are divided into TSS that do (CGI+) or do not (CGI-) overlap with CGIs. Upper right and lower panels show average profiles of H3K115ac, H2K122ac, and H3K27ac ChIP-seq read-density at these same TSS classes. The higher H3K115ac read-density at CGI+ TSS is not due to sample size (Wilcox, p-value<2.2e-16, normalised read coverage within a window spanning TSS+ 500 bp). (G) Average profiles (mean normalised reads) of, (top); 4SU-seq in mESCs centred at protein-coding TSSs (±2 kb) divided into quartiles (Q1–Q4) of 4SU-seq signal within 500 bp upstream and downstream of the TSS for (left) TSS overlapping a CGI (+CGI), or (right) promoters without any CGI (-CGI). Below: H3K115ac ChIP-seq signal around these TSS quartiles defined by 4SU.
Figure 1—figure supplement 1
H3K115ac antibody specificity.
Related to Figure 1. (A) Dot blot for specificity of H3K115ac antibody against unmodified H3K115 and H3K115R peptides and acetylated H3K115 and H3K122 peptides (Key resources table). (B) ChIP-qPCR with H3K115ac antibody from mouse embryonic stem cell (mESC) chromatin spiked with equimolar amounts of bar-coded nucleosome species modified as indicated; acetyl (ac), butyryl (bu), crotonyl (cr), phospho (ph) from the SNAP-ChIP K-acyl-stat panel. The gene body and promoter of Klf4 are included as endogenous targets. Error bars indicate standard deviation from three technical replicates for each of two biological replicates. PCR primer sequences in Supplementary file 4B.
Figure 2 with 1 supplement
Changes in H3K115ac during differentiation.
(A) Boxplots displaying the changes in activity (4SU sequencing [4SU-seq]) of promoters that gain or lose H3K115ac chromatin immunoprecipitation (ChIP) signal across the 7 days of mouse embryonic stem cell (mESC) to neural progenitor cell (NPC) differentiation. Log2 fold change is shown relative to day 0. *Paired Wilcox, p<0.01. (B) Bar plot showing enrichment of gene sets defined based on differential H3K115ac (gain/loss) and differential expression during differentiation (up/down). Enrichments are calculated for CpG island (CGI) and non-CGI promoters. ***Fisher’s exact test p<0.01; n.s. p>0.01, Supplementary file 2a. (C) Aggregate profile plots for 4SU-seq and ChIP-seq data for H3K115ac and H3K27me3 (Mikkelsen et al., 2007) from mESCs and NPCs at promoters with no significant change in H3K115ac occupancy, but significant transcriptional upregulation during differentiation. (D) UCSC genome browser screenshot showing 4SU-seq, ATAC-seq, and ChIP-seq data for H3K115ac and H3K27me3 (Mikkelsen et al., 2007) in mESCs and differentiated NPCs at the Efna5 and Slc22a23 loci. CGIs are indicated. Genome co-ordinates (Mb) are from the mm10 assembly of the mouse genome.
Figure 2—figure supplement 1
H3K115ac dynamics during differentiation.
Related to Figure 2. (A) Aggregate profile plots for 4SU sequencing (4SU-seq) and chromatin immunoprecipitation (ChIP-seq) data for H3K115ac and H3K27me3 (Mikkelsen et al., 2007) at promoters with no significant change in H3K115ac occupancy, or transcription (<2-fold), during differentiation to neural progenitor cells (NPCs). (B) Gene ontology analysis for the background set of genes in Figure 2C. Top 15 biological processes are shown. (C) UCSC genome browser screenshot showing 4SU-seq, ATAC-seq, and ChIP-seq data for H3K115ac and H3K27me3 (Mikkelsen et al., 2007) in mouse embryonic stem cells (mESCs) and differentiated NPCs at the Insm1 locus. CpG islands (CGIs) are indicated. Genome co-ordinates (Mb) are from the mm10 assembly of the mouse genome. (D) Enrichment (log2 observed/expected) of H3K115ac, H3K64ac, H3K122ac, and H3K27ac ChIP signal with polycomb target promoters (H3K27me3) in mESCs. ***p-Value (Fisher’s)<0.01. n.s. not significant (p>0.05). Statistical analysis in Supplementary file 2c. (E) H3K64ac and H3K122ac mESC ChIP-seq profiles at the gene sets that show no change in H3K115ac ChIP signal during ESC to NPC differentiation and that are either transcriptionally upregulated or that show no change in transcription upon differentiation (ChIP-seq data from Pradeepa et al., 2016).
Figure 3 with 1 supplement
H3K115ac is associated with fragile nucleosomes.
(A) Contour plots depicting the high-density regions of chromatin fragments around transcription start site (TSS) (±400 bp) as a function of fragment length (bp) generated from (top) input MNase library, (centre) H3K27ac chromatin immunoprecipitation (ChIP), and (bottom) H3K115ac ChIP. Coverage refers to the proportion of ChIP fragments in the indicated colour-coded contours. The region from 100 bp upstream to the TSS is indicated with dashed lines in red. (B) Mean nucleosome occupancy around mouse TSSs plotted with respect to the nucleosome-depleted region (NDRs), scaled to a length of 500 bp. MNase-seq data (top, West et al., 2014) were used to define NDR as the region between the 3' boundary of –1 nucleosome and the TSS. Mean occupancy of (middle) H3K27ac or (bottom) H3K115ac ChIP-seq fragments is split into sub- and mononucleosomes around the scaled NDRs. (C) Fragment length distribution (bp) of MNase-digested native chromatin fractionated with sucrose gradient sedimentation. Fractions with different nucleosome species (based on the fragment length) were pooled (indicated in parentheses). (D) Input (top) and H3K115ac ChIP-seq (bottom) data, centred at TSS (±1 kb) of most active genes (top 25%) in mouse embryonic stem cells (mESCs), performed on different nucleosome species isolated with sucrose gradient sedimentation from panel C. Data is spike-in normalised.
Figure 3—figure supplement 1
H3K115ac is associated with subnucleosome-sized fragments.
Related to Figure 3. (A) Mean coverage of fragments in MNase-digested input libraries for the most highly active transcription start sites (TSSs) (4SU Q4) and minimally active TSSs (Q1) in mouse embryonic stem cells (mESCs) binned into different fragment lengths (bp). (B) Schematic of selected fragment lengths to define subnucleosomes and mononucleosomes from input libraries. (C) Mean occupancy of H3K115ac (top) or H3K27ac (below) ChIP-seq from mESCs plotted around (±1 kb) TSS. Subnucleosomal and mononucleosomal signals are plotted together with the profile from their respective input libraries. (D) Distribution of fragment lengths (bp) from paired-end libraries for (top) native MNase ChIP-seq of H3K115ac and its input sample, (bottom) H3K27ac ChIP-seq libraries. Distribution is scaled to library size, and the Wilcox test was used to calculate significance. (E) Density profiles of A/T content for input and H3K115ac and H3K27ac ChIP-seq of libraries showing mononucleosomes (monoNuc) and subnucleosomes (subNuc). A/T content does not differ between different input libraries (Wilcox test, p>0.01), but H3K115ac-marked subnucleosomes have a higher A/T content than subnucleosomes marked with H3K27ac (Wilcox test, p<0.01), H3K115ac-marked mononucleosomes have higher A/T content than those with H3K27ac (Wilcox test, p<0.01). The A/T content of sub- and mononucleosomal particles marked with H3K115ac is not significantly different (Wilcox test, p>0.01). Statistical data for panels D and E are in Supplementary file 3a and b, respectively.
Figure 4 with 1 supplement
H3K115ac marks active enhancers.
(A) Heatmap showing the coverage of H3K115ac, H3K122ac, H3K27ac, and ATAC-seq centred on promoter distal accessible peaks (putative enhancers) in mouse embryonic stem cells (mESCs). Data is grouped in enhancers marked by all three H3 acetylation marks (Group 1; H3K27ac+ H3K122ac+ H3K115ac+), just H3K27ac together with H3K122ac (Group 2) or H3K27ac alone (Group 3). (B) Heatmaps showing H3K115ac and ATAC-seq signal for common and dynamic enhancers between ESC and neural progenitor cell (NPC). Loss/gain of H3K115ac correlates with loss/gain in chromatin accessibility. (C) mESC enhancers selected based on the presence of two Oct 4 motifs (n=650) within the Tn5-accessible region, with the region between the two motifs scaled to the same length (shaded grey region). Top: MNase-seq signal (black, left y-axis) and ATAC-seq (purple, right y-axis). H3K115ac ChIP-seq (middle panel) and H3K27ac ChIP-seq (bottom panel) on mononucleosomes (monoNuc; green) or subnucleosome-sized fragments (subMuc; blue). (D) Immunoblotting for H3, H3.3, and H3K115ac on whole-cell extracts from E14 mESCs, H3.3 knock-out ESCs, and the parental ESC line. Ponceau S staining of histones is shown below as loading control (Figure 4—source data 1 and Figure 4—source data 2). A biological replicate blot is shown in Figure 4—figure supplement 1.
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Figure 4—source data 1
Original immunoblots for Figure 4D, indicating the mouse embryonic stem cell (mESC) samples (E14, parental, H3.3KO) and the antibodies used (H4, red; H3, H3.3, and H3K115ac, green).
LI-COR collection data shown below.
- https://cdn.elifesciences.org/articles/108802/elife-108802-fig4-data1-v1.zip
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Figure 4—source data 2
Original files for immunoblots for Figure 4D.
- https://cdn.elifesciences.org/articles/108802/elife-108802-fig4-data2-v1.zip
Figure 4—figure supplement 1
H3K115ac correlates with regulatory activity at mouse embryonic stem cell (mESC) enhancers.
Related to Figure 4. (A) Overlap of STARR-seq+ve sequences (Peng et al., 2020) with sites corresponding to open (ATAC+) or closed (ATAC–) chromatin sites in the mESC genome, and for different mESC histone acetyl-lysine peaks. ‘None’ indicates STARR-seq active sequences with no overlap with the indicated post-translational modification class. H2B-NTac refers to regions marked with at least one of the acetyl-lysines in the N-terminal of histone H2B (K5, K11, K12, K16, and K20, Narita et al., 2023). (B) The proportion of peaks for different histone acetylation marks that are defined as open or closed by ATAC-seq in mESCs. (C) A random forest model was trained to predict H3K115ac-positive vs. -negative peaks (but marked by H3K27ac and/or H3K122ac) based on ChIP-seq overlap. SHAP values were calculated to determine the impact on the model (top 20 features shown, left). The prediction confusion matrix is shown for the test data (right). (D) Bar plot showing % of promoter- or enhancer-associated peaks in mESC and neural progenitor cells (NPCs). Nearly 33% of all H3K115ac peaks are associated with promoters in both ESCs and NPCs, with 70% of them common between ESCs and NPCs. In contrast, the majority of dynamic H3K115ac peaks are associated with enhancers (ESC-specific; n=1881, NPC-specific; n=2811). (E) ATAC-seq signal around Oct4-occupied enhancers in mESCs divided into quartiles (Q1-Q4, low to high) of Oct4 ChIP-seq peak strength. (F) H3K115ac (left) and H3K27ac (right) paired-end ChIP signal around Oct4-occupied enhancers. ChIP-seq reads are separated according to fragment length into mononucleosomes (green; monoNuc) and subnucleosomes (blue; subNuc). (G) Heatmap depicting H3.3 turnover index (Deaton et al., 2016; GSM2080325_TI_ES.wig in GEO accession GSE78910) centred for H3K115ac-+ve and –ve regions. (H) Biological replicate for Figure 4D. Immunoblotting for H3K115ac, H3.3, and H3 (green), and H4 (red) on whole-cell extracts from E14 mESCs, H3.3 knock-out ESCs, and the parental ESC line. Red size markers are also shown (Figure 4—figure supplement 1—source data 1 and 2).
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Figure 4—figure supplement 1—source data 1
Original immunoblots for lower panel indicating the mouse embryonic stem cell (mESC) samples (E14, parental, H3.3KO) and the antibodies used (H4, red; H3, H3.3, and H3K115ac, green; β-tubulin, green).
The gel was cut horizontally and the top half probed with antibody detecting β-tubulin as a loading control. The lower half has probed for H3/H4. LI-COR collection data shown below.
- https://cdn.elifesciences.org/articles/108802/elife-108802-fig4-figsupp1-data1-v1.zip
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Figure 4—figure supplement 1—source data 2
Original files for immunoblots for Figure 4—figure supplement 1b.
- https://cdn.elifesciences.org/articles/108802/elife-108802-fig4-figsupp1-data2-v1.zip
Figure 5 with 1 supplement
H3K115ac marks fragile nucleosomes at sites of high CTCF occupancy.
(A) Mean occupancy of nucleosomes derived from MNase-seq (from West et al., 2014) around CTCF sites across the four quartiles of CTCF ChIP-seq peak strength. All CTCF motifs are oriented from 5’ to 3’ (left to right). Positions of first flanking upstream (–1) and downstream nucleosome (–1) positions are marked. (B) H3K115ac ChIP-seq signal from (top) mononucleosomal- and (bottom) subnucleosomal-sized fragments in mouse embryonic stem cells (mESCs) around CTCF motifs across the four quartiles of CTCF ChIP-seq peak strength as in (A). (C) Contour plots depicting high-density regions of (left) input, (centre) H3K115ac ChIP, (right) H3K27ac ChIP paired-end sequenced MNase fragments around top (Q4) and bottom (Q1) quartiles of CTCF ChIP-seq peaks in mESCs (data from Mas et al., 2018) as a function of fragment length. All CTCF motifs are oriented in the same direction.
Figure 5—figure supplement 1
H3K27ac and H3K115ac relative to CTCF binding sites and motif orientation.
Related to Figure 5. (A) H3K27ac ChIP-seq signal from mononucleosomal (top) and subnucleosomal (bottom) sized fragments in mouse embryonic stem cells (mESCs) around CTCF motifs across the four quartiles of CTCF ChIP-seq peak strength. All CTCF motifs are oriented from 5’ to 3’ (left to right). (B) Heatmap of MNase-seq data ranked by quartiles of CTCF occupancy with CTCF motifs oriented in the same (left) direction or randomised orientation (middle). (C) As in (B) but divided into quartiles (Q1–Q4) of distance to the closest TAD boundary in mESCs (TAD boundaries from Bonev et al., 2017). Median distance (kb) to TAD boundary for each quartile is shown on the right; minimum and maximum distances are shown in parentheses. Within each TAD quartile, sites are sorted by CTCF occupancy in descending order.
Author response image 1
Tables
Key resources table
| Reagent type (species) or resource | Designation | Source or reference | Identifiers | Additional information |
|---|---|---|---|---|
| Cell line (Mus musculus) | E14tg2A | Williamson et al., 2023 | Mouse embryonic stem cell line | |
| Cell line (Mus musculus) | 46C Sox1-GFP | Ying et al., 2003; Benabdallah et al., 2019 | Mouse embryonic stem cell line | |
| Cell line (Mus musculus) | DPY30 miniAID | Wang et al., 2023 | Mouse embryonic stem cell line | |
| Other | DMEM/F12 | Gibco | #31330-032 | Cell culture media |
| Other | Neuro basal medium | Gibco | #21103-049 | Cell culture media |
| Other | B27 | Invitrogen | #17504044 | Cell culture media |
| Other | N-2 supplement | Invitrogen | #17502048 | Cell culture media |
| Antibody | Anti-H3K115ac (Rabbit polyclonal IgG) | PTM Bio USA | # PTM-170 | 1:1500 dilution for immunoblot; no dilution for ChIP |
| Antibody | Anti-H3K27ac (Rabbit polyclonal IgG) | Abcam | RRID:AB_2118291 | No dilution for ChIP |
| Antibody | HRP-linked anti-Rabbit IgG (Goat polyclonal) | Cell Signalling Technology | RRID:AB_2099233 | 1:10,000 dilution for immunoblot |
| Antibody | Anti-H3.3 (Rabbit polyclonal) | Millipore | RRID:AB_10845793 | 1:1000 for immunoblot |
| Antibody | Anti-H3 (Rabbit polyclonal) | Abcam | RRID:AB_302613 | 1:5000 for immunoblot |
| Antibody | Anti-H4 (Mouse monoclonal) | Cell Signalling Technology | RRID:AB_1147658 | 1:3000 for immunoblot |
| Antibody | IRDye 800CW Goat anti-Rabbit | LI-COR | t926-32211 | 1:20,000 for immunoblot |
| Antibody | IRDye 680RD Goat anti-mouse | LI-COR | t926-68070 | 1:10,000 for immunoblot |
| Chemical compound, drug | 2-Mercaptoethanol | Gibco | #31350010 | |
| Chemical compound, drug | 4-Thiouridine | Sigma | T4509 | |
| Chemical compound, drug | TRIzol | Invitrogen | 15596026 | |
| Chemical compound, drug | Biotin-HPDP | Pierce | 21341 | |
| Chemical compound, drug | CAIHAKRVTIMK | Thermo Fisher | Custom H3K115 peptide | |
| Chemical compound, drug | CAIHARRVTIMK | Thermo Fisher | Custom H3K115R peptide | |
| Chemical compound, drug | CAIHAK[Ac]RVTIMPK | Thermo Fisher | Custom H3K115ac peptide | |
| Chemical compound, drug | CGGVTIMPK[Ac]DIQLA | Thermo Fisher | Custom H3K122ac peptide | |
| Commercial assay or kit | SuperSignal West Femto Maximum Sensitivity Substrate | Thermo Fisher | # 34096 | HRP detection |
| Commercial assay or kit | 4–20% TGX Gel | Bio-Rad | #4561094 | Pre-cast polyacrylamide gel |
| Commercial assay or kit | SNAP-ChIP K-AcylStat Panel | Epicypher | # 19-3001 | |
| Commercial assay or kit | MNase | New England Biolabs | M0247S | |
| Commercial assay or kit | Dynabeads Protein-A | Invitrogen | 10001D | |
| Commercial assay or kit | Tn5 | Illumina | # 20034197 | |
| Commercial assay or kit | AMPure XP beads | Beckman | A63880 | |
| Commercial assay or kit | Qubit assay | Invitrogen | Q32851 | |
| Commercial assay or kit | Turbo DNA-free | Invitrogen | AM1907M | DNase |
| Commercial assay or kit | µMacs Streptavidin beads | Miltenyi | 130-074-101 | |
| Commercial assay or kit | RNeasy MinElute cleanup kit | QIAGEN | 74204 | |
| Commercial assay or kit | RiboMinus eukaryote system v2 | Ambion | A15027 | |
| Commercial assay or kit | NEBNext Ultra II directional RNA library preparation kit | New England Biolabs | E7760 | |
| Commercial assay or kit | NEBNext Ultra II DNA library kit | New England Biolabs | E7645 | |
| Commercial assay or kit | MinElute PCR Purification Kit | QIAGEN | 28004 | |
| Software, algorithm | SRA toolkit (v3.0.5) | https://www.ncbi.nlm.nih.gov/sra | Kodama et al., 2012 | |
| Software, algorithm | fastp (v0.23.4) | https://github.com/OpenGene/fastp | Chen et al., 2018; Chen, 2026 | |
| Software, algorithm | bowtie2 (v2.5.3) | https://sourceforge.net/projects/bowtie-bio/ | Langmead and Salzberg, 2012 | |
| Software, algorithm | SAMtools (v1.20) | https://github.com/samtools/samtools | Danecek et al., 2021; Bonfield et al., 2026 | |
| Software, algorithm | Picard (v2.25.1) | https://broadinstitute.github.io/picard/ | http://broadinstitute.github.io/picard/, Broad Institute, | |
| Software, algorithm | Bedtools (v2.31.1) | https://bedtools.readthedocs.io/en/latest/ | Quinlan and Hall, 2010 | |
| Software, algorithm | HOMER (v1.0) | http://homer.ucsd.edu/homer/ | Heinz et al., 2010 | |
| Software, algorithm | wigTobigWig (v2.9) | https://www.encodeproject.org/software/wigtobigwig/ | Lee et al., 2022 | |
| Software, algorithm | DESeq2 (v1.50.2) | https://bioconductor.posit.co/packages/3.19/bioc/html/DESeq2.html | Love et al., 2014 | |
| Software, algorithm | DANPOS3 (v1.0) | https://github.com/sklasfeld/DANPOS3 | Chen et al., 2013; Klasfeld, 2026 | |
| Software, algorithm | deepTools (3.5.1) | https://deeptools.readthedocs.io/en/latest/ | Ramírez et al., 2016 | |
| Software, algorithm | PeakPredict (v0.1) | https://github.com/efriman/PeakPredict | Friman, 2024b | |
| Software, algorithm | matchPWM (v2.78.0) | https://github.com/Bioconductor/Biostrings/blob/devel/R/matchPWM.R | Pagès et al., 2025; Pagès, 2013; https://doi.org/10.18129/B9.bioc.Biostrings | |
| Software, algorithm | ggdensity (v1.0.1) | https://jamesotto852.github.io/ggdensity/ | Otto and Kahle, 2023 |
Additional files
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Supplementary file 1
Pearson’s correlation between biological replicates and sequencing mode (single vs. paired end) for MNase-digested input, H3K27ac and H3K115ac ChIP-seq, and ATAC-seq datasets generated in this study from undifferentiated mouse embryonic stem cells (mESCs) and from mESCs differentiated into neural progenitor cells (NPCs).
Data are available in NCBI GEO with the Accession number GSE246191.
- https://cdn.elifesciences.org/articles/108802/elife-108802-supp1-v1.xlsx
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Supplementary file 2
Fisher’s exact test for data related to Figure 2, Figure 2—figure supplement 1.
(a) Association of gain/loss of H3K115ac with transcriptional changes (up or down) during embryonic stem cell (ESC) to neural progenitor cell (NPC) differentiation for: All promoters, and promoters with or without CpG islands (CGIs). The number of genes is indicated. Data relevant to Figure 2B. (b) As in (a) but also for bivalent genes from Seneviratne et al., 2024, and including promoters of genes that show no change (nc) in H3K115ac during differentiation. (c) Association of H3K115ac, H3K64ac, H3K122ac, and H3K27ac post-translational modification (PTM) ChIP-seq peaks in mESCs with: All CGI promoters, promoters of bivalent genes from Seneviratne et al., 2024, promoters occupied by Ezh2. Data relevant to Figure 2—figure supplement 1D.
- https://cdn.elifesciences.org/articles/108802/elife-108802-supp2-v1.xlsx
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Supplementary file 3
Wilcox’s test for data related to Figure 3—figure supplement 1.
(a) Statistical data (Wilcox test) for data in Figure 3—figure supplement 1D comparing paired-end fragment length between H3K115ac and H3K27ac chromatin immunoprecipitation (ChIP) with the relevant input chromatin (for two biological replicates). (b) Statistical data (Wilcox test) for data in Figure 3—figure supplement 1E comparing AT content between ChIP-seq mono- or subnucleosome-sized paired-end fragment lengths for H3K115ac or H3K27ac ChIP data.
- https://cdn.elifesciences.org/articles/108802/elife-108802-supp3-v1.xlsx
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Supplementary file 4
Supplementary data for methods.
(a) Sequences of (top) guide RNAs to excise the exon 2 of H3f3a and exons 3 and 4 of H3f3b and (below) genotyping primers for H3.3KO DPY30-miniAID mouse embryonic stem cells (mESCs) (Wang et al., 2023).
- https://cdn.elifesciences.org/articles/108802/elife-108802-supp4-v1.xlsx
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MDAR checklist
- https://cdn.elifesciences.org/articles/108802/elife-108802-mdarchecklist1-v1.docx
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Acetylation of H3K115 is associated with fragile nucleosomes at CpG island promoters and active regulatory sites
eLife 14:RP108802.
https://doi.org/10.7554/eLife.108802.3
