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BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responses [RNA-seq]

GSE318083 Homo sapiens (human) RNA-seq (gene expression) 43 samples Submitted 2026/04/10 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 43 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
43 samples: 21 conditions, mostly in duplicateGroups 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.
Paper
BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responsesbioRxiv : the preprint server for biology · 2026
Summary (written by the submitters)
Gene regulation relies on cis-regulatory sequence elements (cREs), including enhancers, to alter gene expression in response to developmental and environmental cues. BRG1/BRM-Associated Factors (BAF) chromatin remodeling complexes are required to maintain an “accessible” chromatin state at many cREs, which enables binding by transcription factors (TFs) and other regulatory proteins.
Read the full summary ↓
However, cREs exhibit a broad range of sensitivity to loss of BAF function, and the basis of this variable dependence on BAF remains unclear. To identify the characteristics of cREs that rely on BAF complexes to maintain chromatin accessibility, we generated time- and dosage-resolved maps of chromatin accessibility changes following acute BAF inhibition in the lymphoblastoid cell line GM12878. We then integrated these results with ChIP-seq data on more than one hundred TFs and histone modifications available for this cell line and used machine learning to identify features that predict changes in chromatin accessibility upon BAF inhibition. We found that several TFs were associated with sensitivity to BAF inhibition, including widely expressed Activator Protein 1 (AP-1) factors and lymphoid lineage-defining TFs such as RUNX3 and PU.1. Surprisingly, we also found that cREs bearing the chromatin signature of “primed” enhancers – characterized by H3K4me1 enrichment in the absence of the “active” enhancer mark H3K27ac – were significantly more sensitive to BAF inhibition than typical active enhancers. Nearly all primed enhancers lost chromatin accessibility within 30 minutes of BAF inhibition. Notably, primed enhancers are known to facilitate transcriptional responses to external stimuli. Thus, we reasoned that BAF function may be required for cells to mount transcriptional stimulus responses. To test this theory, we assessed the effect of acute BAF inhibition on responses to two orthogonal stimuli, interferon gamma and dexamethasone. We found that BAF inhibition was sufficient to prevent chromatin and transcriptional responses to these stimuli. cREs which normally gained accessibility in response to stimulation failed to do so with BAF inhibition, and these cREs were linked to genes with suppressed transcriptional induction upon stimulation. Collectively, our results demonstrate a requirement for continuous BAF activity to enable stimulus response and suggest that defective signal responsiveness may be a pathogenic mechanism in disease states caused by loss-of-function mutations in BAF subunits.
Published in
BAF complexes maintain accessibility at stimulus-responsive chromatin and are required for transcriptional stimulus responses
Gulka AOD, Kang KA, Zhou Z et al. · bioRxiv : the preprint server for biology 2026 · PMID 41890073 · doi:10.64898/2026.03.19.712964
This dataset
Open GSE318083 in finder → Find more human RNA-seq datasets →
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.

Series matrix ↓
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 GSE318083_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
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.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1416432 and SRA study SRP670645. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41890073) ↗
Study design
21 conditions, mostly in duplicate
HepG2 RNA-seq library, DMSO , 24h , ×2 HepG2 RNA-seq library, BRM014 (10uM) , 24h , ×2 GM12878 RNA-seq library, DMSO , 6h , ×2 GM12878 RNA-seq library, PBS , 6h , ×2 GM12878 RNA-seq library, TNF , 6h , ×2 GM12878 RNA-seq library, LPS , 6h , ×2 GM12878 RNA-seq library, IL2 , 6h , ×2 GM12878 RNA-seq library, IFNg , 6h , ×2 +14 more

Supports a between-group comparison across 42 samples.

How we read this: 21 replicated groups read from 43 sample titles; they account for 42 of them. 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

+ 3 more — browse all 43 samples with per-sample file links →

Datasets on a similar topic

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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.