GEO series
The Heme-regulated transcriptional repressor, BACH1 safeguards macrophage enhancer selection, activation andtissue adaptation [ATAC-seq_BMDM]
GSE245645
Mus musculus (mouse)
ChIP-seq / ATAC-seq (genome binding and open chromatin)
12 samples
Submitted 2026/07/13
Platform GPL17021
At a glance
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 samples
- What it is
- ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
- Organism
- Mus musculus (mouse)
- Samples
- 12 samples: 12 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
- Data you can get
- A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Transcriptional master regulators of the myeloid lineage (like PU.1, Cebpa/b, etc.) are believed to be the main drivers of chromatin reprogramming during differentiation and polarization. Such developmental transcription factors act via their pioneer ability to open chromatin de novo and bookmark genomic regulatory sites (enhancers and promoters) to later recruit signal-dependent TFs, co-factors, and the basal transcriptional machinery.
Read the full summary ↓
However, recent studies by us and others challenged this “developmental TF-centric” mode as they suggested that signal-dependent TFs, particularly repressors, can also have a pioneer and thus safeguarding role in the MF epigenome at baseline and during acute inflammation. Such an expanded model predicts that active transcriptional repression and chromatin bookmarking by signal-dependent master regulators are key mechanisms for safeguarding the enhancer repertoire and proper priming, deployment, and resolution of an inflammatory response. Here, we show that BACH1, a heme-sensitive transcriptional repressor, acts as such a pervasive epigenomic safeguard to regulate tissue macrophage identity. We show that BACH1 is part of the core hardwired transcriptional program of ground-state macrophages shaping the chromatin accessibility of thousands of distal regulatory elements. Furthermore, BACH1 cistrome is extensive, not static but dynamic, and expanding upon different inflammatory stimuli and correlates with pre-formed and de novo formed enhancer-promoter networks. We further show that myeloid BACH1 is indispensable in vivo for tissue regeneration upon injury as it regulates the kinetics of Ly6C+ to Ly6C- transition of inflammatory macrophages and regulates the onset, the kinetics and magnitude of expression of critical inflammatory and repair-related genes. Finally, BACH1 was found to be required in vivo for competitive fitness and tissue adaptation of several tissue-resident macrophage populations (eg. lung, peritoneal macrophages), further supporting its pervasive role in acquiring and maintaining the functional specificity and diversity of tissue macrophages. Taken together, our data suggest that BACH1 acts as a signal-dependent master regulator that directly controls key transcriptional circuits during tissue macrophage subtype function, specification and inflammatory responses in vivo.
This dataset
Download · which file do I need?
Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.
1 · Just have a look
Processed table
The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.
2 · Re-analyse it
Supplementary files
The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE245645_RAW.tar (it can run to tens of gigabytes).
3 · Start from the raw reads
Raw sequencing reads
The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.
What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.
Also filed as BioProject PRJNA1029495 and SRA study SRP466993. Searching any of these in the dataset finder brings you back here.
Study design
12 samples, each with a distinct title — no replicated groups
Supports a case/control comparison: 2 samples read as cases, 4 as controls.
How we read this: Read from 12 sample titles: 12 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.
Samples in this study
- GSM7846341 ATAC-seq in wild type mouse bone marrow derived macrophages unstim (rep1)
- GSM7846342 ATAC-seq in wild type mouse bone marrow derived macrophages unstim (rep2)
- GSM7846343 ATAC-seq in Bach1-deficient mouse bone marrow derived macrophages unstim (rep1)
- GSM7846344 ATAC-seq in Bach1-deficient mouse bone marrow derived macrophages unstim (rep2)
- GSM7846345 ATAC-seq in wild type mouse bone marrow derived macrophages veh (rep1)
- GSM7846346 ATAC-seq in wild type mouse bone marrow derived macrophages veh (rep2)
- GSM7846347 ATAC-seq in wild type mouse bone marrow derived macrophages treated with 100 uM heme (rep1)
- GSM7846348 ATAC-seq in wild type mouse bone marrow derived macrophages treated with 100 uM heme (rep2)
- GSM7846349 ATAC-seq in Bach1-deficient mouse bone marrow derived macrophages veh (rep1)
- GSM7846350 ATAC-seq in Bach1-deficient mouse bone marrow derived macrophages veh (rep2)
- GSM7846351 ATAC-seq in Bach1-deficient mouse bone marrow derived macrophages treated with 100 uM heme (rep1)
- GSM7846352 ATAC-seq in Bach1-deficient mouse bone marrow derived macrophages treated with 100 uM heme (rep2)
Datasets on a similar topic
- GSE245648 The Heme-regulated transcriptional repressor, BACH1 safeguards macrophage enhancer selection, activation andtissue adaptation [RNA-seq_BMDM] 24 samples shares bach1, bmdm, heme-regulated, safeguards, macrophage, activation, adaptation, repressor
- GSE245647 The Heme-regulated transcriptional repressor, BACH1 safeguards macrophage enhancer selection, activation andtissue adaptation [ChIP-seq] 62 samples shares bach1, heme-regulated, safeguards, macrophage, activation, adaptation, repressor
- GSE245646 The Heme-regulated transcriptional repressor, BACH1 safeguards macrophage enhancer selection, activation andtissue adaptation [ATAC-seq_muscle] 22 samples shares bach1, heme-regulated, safeguards, macrophage, activation, adaptation, repressor
- GSE245649 The Heme-regulated transcriptional repressor, BACH1 safeguards macrophage enhancer selection, activation andtissue adaptation [RNA-seq_muscle] 11 samples shares bach1, heme-regulated, safeguards, macrophage, activation, adaptation, repressor
- GSE245650 The Heme-regulated transcriptional repressor, BACH1 safeguards macrophage enhancer selection, activation andtissue adaptation [Capture Hi-C] 6 samples shares bach1, heme-regulated, safeguards, macrophage, activation, adaptation, repressor
- GSE245651 BACH1 acts as a pioneer repressor to enable macrophage plasticity and adaptation across tissues and inflammatory contexts 165 samples shares bach1, macrophage, adaptation, repressor
- GSE327645 BACH1 acts as a pioneer repressor to enable macrophage plasticity and adaptation across tissues and inflammatory contexts [RNA-seq/ATAC-seq] 28 samples shares bach1, macrophage, adaptation, repressor
- GSE289356 Effects of type I IFN signaling on gene expression of Mycobacterium tuberculosis-infected bone marrow-derived macrophages (BMDMs) 34 samples shares bmdm, macrophage
Share this dataset
Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.