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Mechanistic basis of gene regulation by SRCAP and H2A.Z (RNA-Seq)

GSE269309 Mus musculus (mouse) RNA-seq (gene expression) 30 samples Submitted 2026/01/06 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 30 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
Mus musculus (mouse)
Samples
30 samples
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
Mechanisms of gene regulation by SRCAP and H2A.ZNature communications · 2026
Summary (written by the submitters)
Discriminating regulatory functions of chromatin composition from those of chromatin-modifying complexes is a central problem in gene regulation. This question remains unexplored in the context of histone variants and their dedicated chromatin remodelers. Here we dissect the distinct and cell cycle-dependent functions of Snf2 Related CREBBP Activator Protein (SRCAP) and H2A.Z in gene regulation of pluripotent stem cells.
Read the full summary ↓
Using acute degradation of endogenous SRCAP, we uncover dynamic changes of H2A.Z occupancy and continuous requirement of SRCAP over the cell cycle. We also engineered an SRCAP mutant, defective for H2A.Z deposition, allowing us to distinguish H2A.Z-dependent and independent functions of SRCAP. We discover that SRCAP exhibits essential H2A.Z-independent functions in inhibiting DNA binding of dozens of pioneer transcription factors at enhancers by steric hindrance. In contrast, H2A.Z acts mainly as a transcriptional repressor gatekeeping the expression of lineage-specific genes. Our study establishes the catalytic-independent role of a chromatin remodeler in broadly regulating transcription factor binding, and demonstrates how a chromatin remodeler-histone variant pair orchestrates transcription to maintain self-renewal and plasticity of pluripotent stem cells.
Published in
Mechanisms of gene regulation by SRCAP and H2A.Z
Tollenaere A, Ugur E, Dalla Longa S et al. · Nature communications 2026 · PMID 41792122 · doi:10.1038/s41467-026-70087-x
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 GSE269309_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: 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 PRJNA1120936 and SRA study SRP512307. Searching any of these in the dataset finder brings you back here.

Samples in this study

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