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
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
28 samples
Submitted 2026/07/09
Platform GPL13112
Summary
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. 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
Direct links to NCBI, no account and no request form: the whole study as GSE327645_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 28 samples. Raw sequencing reads are also available from 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 conditions, each sampled once — no replicated groups
Read from 28 sample titles: 28 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- 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)
Similar datasets
- GSE217664 Decoding Trp53 regulatory program in various tissues and organs 404 samples
- GSE312302 NMuMG PBRM1 RNA-seq, ATAC-seq, and ChIP-seq 171 samples
- GSE306265 Astrocyte glucocorticoid receptor signaling restricts neuronal plasticity 106 samples
- GSE201132 Macrophage 58 samples
- GSE290756 Lineage Plasticity Driven by GATA6 Loss Fuels Colorectal Cancer Metastasis 50 samples
- GSE243165 Signal-responsive transcription factors cooperate to establish alveolar macrophage identity 42 samples
- GSE292377 Step-wise signal integration governs adaptive programming of lymphocytes [bulkRNA-seq and ATAC-seq] 41 samples
- GSE190309 Single nuclei RNA and ATAC sequencing of mouse trigeminal ganglia at baseline and in atopic dermatitis-like disease. 14 samples
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.