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Linker histone H1.0 and JUNB Interaction Maintains Lineage-Specific and Age-Dependent Chromatin Architecture to Safeguard Cell Identity [ATAC-seq]

GSE338103 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2026/07/17 Platform GPL34475Platform GPL34295
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 14 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
Homo sapiens (human)
Samples
14 samples: 6 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.
Summary (written by the submitters)
Maintenance of differentiated cell identity is essential for tissue homeostasis and depends on active molecular mechanisms that reinforce cell fate stability. This thesis focuses on identifying the molecular factors involved in this maintenance system and defining how they function as barriers that oppose cell fate reprogramming and protect cellular identity.
Read the full summary ↓
More broadly, this work addresses a fundamental question in biology: how differentiated cells actively preserve their identity while resisting inappropriate lineage programs, and how aging erodes these mechanisms, contributing to loss of cell identity in aged cells. In particular, this work examines how transcription factor barriers cooperate with chromatin regulators to maintain cell fate stability. In a previous study, JUNB was identified as a transcription factor barrier that restricts cell fate reprogramming through regulation of chromatin accessibility at both open and closed chromatin regions. Notably, transcription factors are not typically characterized for their ability to regulate closed chromatin states. Given that transcription factors frequently function in cooperation with other regulatory proteins, it was hypothesized that JUNB interacts with additional chromatin regulators to control chromatin accessibility more broadly. In this study, H1F0, a linker histone with chromatin-regulatory properties, was identified as a novel functional interactant of JUNB that acts as a barrier to cell fate reprogramming. Mechanistic investigation further demonstrated that JUNB and H1F0 cooperate at shared regulatory regions, including sites associated with the chromatin architectural regulator CTCF, to modulate chromatin accessibility. Through this coordinated action, engagement of lineage-reprogramming transcription factors with gene programs required for alternative fate activation was restricted, thereby preserving cell fate stability.
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 GSE338103_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 PRJNA1492512 and SRA study SRP716622. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
ATAC-iMGT-Myh6-eGFP-MEFs, siControl, D1, Biol ×2 ATAC-iMGT-Myh6-eGFP-MEFs, siJunb, D1, Biol ×2 ATAC-iMGT-Myh6-eGFP-MEFs, siH1f0, D1, Biol ×2 ATAC-iMYOD-IMR90, siCTRL, D1, Biol ×2 ATAC-iMYOD-IMR90, siJUNB, D1, Biol ×2 ATAC-iMYOD-IMR90, siH1F0, D1, Biol ×2 ATAC-iMGT-Myh6-eGFP-MEFs, siControl, Ground s… ×1 ATAC-iMGT-Myh6-eGFP-MEFs, siControl, Ground … ×1

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 14 sample titles; they account for 12 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
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