GEO series
BACH1 acts as a pioneer repressor to enable macrophage plasticity and adaptation across tissues and inflammatory contexts [RNA-seq/ATAC-seq]
GSE327645
Mus musculus (mouse)
ChIP-seq / ATAC-seq (genome binding and open chromatin)
28 samples
Submitted 2026/07/09
Platform GPL13112
At a glance
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 28 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
- 28 samples: 28 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 GSE327645_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 PRJNA1451756 and SRA study SRP690848. Searching any of these in the dataset finder brings you back here.
Study design
28 samples, each with a distinct title — no replicated groups
Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.
How we read this: Read from 28 sample titles: 28 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
- GSM9662562 RNA-seq in wild-type alveolar macrophages from bone marrow-chimeric mice (rep1)
- GSM9662563 RNA-seq in wild-type alveolar macrophages from bone marrow-chimeric mice (rep2)
- GSM9662564 RNA-seq in wild-type alveolar macrophages from bone marrow-chimeric mice (rep3)
- GSM9662565 RNA-seq in Bach1 cKO alveolar macrophages from bone marrow-chimeric mice (rep1)
- GSM9662566 RNA-seq in Bach1 cKO alveolar macrophages from bone marrow-chimeric mice (rep2)
- GSM9662567 RNA-seq in Bach1 cKO alveolar macrophages from bone marrow-chimeric mice (rep3)
- GSM9662568 ATAC-seq in wild-type alveolar macrophages (rep1)
- GSM9662569 ATAC-seq in wild-type alveolar macrophages (rep2)
- GSM9662570 ATAC-seq in wild-type alveolar macrophages (rep3)
- GSM9662571 ATAC-seq in Bach1 cKO alveolar macrophages (rep1)
- GSM9662572 ATAC-seq in Bach1 cKO alveolar macrophages (rep2)
- GSM9662573 ATAC-seq in Bach1 cKO alveolar macrophages (rep3)
- GSM9662574 RNA-seq in control (empty vector) wild-type bone marrow-derived macrophages untreated (rep1)
- GSM9662575 RNA-seq in BACH1-overexpressing (BACH1 cDNA vector) wild-type BMDMs treated with LPS (4h) (rep1)
- GSM9662576 RNA-seq in BACH1-overexpressing (BACH1 cDNA vector) wild-type BMDMs treated with LPS (4h) (rep2)
- GSM9662577 RNA-seq in BACH1-overexpressing (BACH1 cDNA vector) wild-type BMDMs treated with LPS (4h) (rep3)
- GSM9662578 RNA-seq in BACH1-overexpressing (BACH1 cDNA vector) wild-type BMDMs untreated (rep2)
- GSM9662579 RNA-seq in BACH1-overexpressing (BACH1 cDNA vector) wild-type BMDMs untreated (rep1)
- GSM9662580 RNA-seq in control (empty vector) wild-type BMDMs untreated (rep2)
- GSM9662581 RNA-seq in control (empty vector) wild-type BMDMs treated with LPS (4h) (rep1)
- GSM9662582 RNA-seq in control (empty vector) wild-type BMDMs treated with LPS (4h) (rep2)
- GSM9662583 RNA-seq in control (empty vector) wild-type BMDMs treated with LPS (4h) (rep3)
- GSM9662584 ATAC-seq in BACH1-overexpressing wild-type BMDMs (rep1)
- GSM9662585 ATAC-seq in BACH1-overexpressing wild-type BMDMs (rep2)
- GSM9662586 ATAC-seq in BACH1-overexpressing wild-type BMDMs (rep3)
- GSM9662587 ATAC-seq in control (empty vector) wild-type BMDMs (rep1)
- GSM9662588 ATAC-seq in control (empty vector) wild-type BMDMs (rep2)
- GSM9662589 ATAC-seq in control (empty vector) wild-type BMDMs (rep3)
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, macrophage, adaptation, repressor
- GSE262721 Targeting plasticity in the pyrimidine synthesis pathway potentiates macrophage-mediated phagocytosis in pancreatic cancer models 10 samples shares macrophage, plasticity
- GSE237954 Oncofetal reprogramming drives phenotypic plasticity in WNT-dependent colorectal cancer 122 samples shares plasticity
- GSE306265 Astrocyte glucocorticoid receptor signaling restricts neuronal plasticity 106 samples shares plasticity
- GSE201132 Macrophage 58 samples shares macrophage
- GSE290756 Lineage Plasticity Driven by GATA6 Loss Fuels Colorectal Cancer Metastasis 50 samples shares plasticity
- GSE243165 Signal-responsive transcription factors cooperate to establish alveolar macrophage identity 42 samples shares macrophage
- GSE215963 Subclonal evolution revealed by single-cell profiles of expressed mutations identifies adaptation mechanisms to immunotherapy in melanoma. 1497 samples shares adaptation
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.