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Transcription-dependent heterochromatin at the Xist promoter shapes the random choice of the inactive X chromosome [Xist-Tsix-perturbations_CutnTag]

GSE339202 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 42 samples Submitted 2026/07/25 Platform GPL34475Platform GPL28457
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 42 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
42 samples: 14 conditions, mostly in triplicateGroups 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)
In female mammals, Xist, the master regulator of X-chromosome inactivation (XCI), is expressed monoallelically. This pattern is established during early embryonic development, when the active Xist allele is chosen at random in each cell. How this choice is made remains incompletely understood. Here we identify a role for the repressive chromatin mark H3K9me3 in the initiation of XCI by combining knock-down and overexpression strategies in differentiating mouse embryonic stem cells, which recapitulate the onset of random XCI.
Read the full summary ↓
We show that H3K9me3 accumulates at the promoter-proximal region of the silent Xist allele in female cells at the same time when the monoallelic Xist expression is established. Unexpectedly, we find that H3K9me3 accumulation requires prior transcription of Xist itself. This is likely to occur during the initial phase of Xist upregulation, when Xist is frequently transcribed also in male cells and from both X chromosomes in females. A repressive function of Xist-dependent H3K9me3 accumulation is supported by our finding that premature, transient Xist overexpression primes an allele for future silencing and thereby skews the choice of the inactive X. Xist-dependent H3K9me3 recruitment does not require transcription of its antisense transcript Tsix, which can however enhance subsequent maintenance of the mark. In addition, the X-linked Xist activator RNF12 counteracts H3K9me3 formation at the locus independently of its known target REX1. Our results thus suggest an important role of facultative heterochromatin formation in the choice process at the onset of XCI. Activation and repression mechanisms are intertwined, to ensure the silencing of one Xist allele and the activation of the other within each female cell.
This dataset
Open GSE339202 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE339202_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1497982 and SRA study SRP719614. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
14 conditions, mostly in triplicate
CasTuner XX sgTsix KD Day4 ×3 CasTuner XX sgTsix ctrl Day4 ×3 CasTuner XX sgXist KD Day4 ×3 CasTuner XX sgXist ctrl Day4 ×3 XXdXIC XistOverexpression ESC ×3 XXdXIC ctrl ESC ×3 XXdXIC XistOverexpression Day2 ×3 XXdXIC ctrl Day2 ×3 +6 more

Supports a case/control comparison: 6 samples read as cases, 21 as controls.

How we read this: 14 replicated groups read from 42 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

+ 2 more — browse all 42 samples with per-sample file links →

Datasets on a similar topic

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