GEO series

Deletion of Xist repeat B disrupts cell cycle and asymmetric cell division through Usp9x hyperactivation in mice [II]

GSE278344 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 23 samples Submitted 2025/02/14 Platform GPL21273

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 23 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: 23 samples: 8 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.
Paper: Deletion of Xist repeat B disrupts cell cycle and asymmetric cell division through Usp9x hyperactivation in miceNucleic acids research · 2025

Summary (written by the submitters)

During X-inactivation (XCI), Xist RNA establishes silencing by coating the chromosome in cis and binding diverse proteins to promote formation of a heterochromatic domain. However, Xist repeat B role beyond initiation of XCI remains unclear. Here, we ﬁnd that loss of Xist repeat B in female mice allows survival and leads to a small body size persisting throughout life.

Read the full summary ↓

Epigenetic and transcriptomic analyses reveal low levels of H3K27me3 and H2AK119ub occupancy on the X chromosome, except in certain CpG island regions, and partial reactivation of X-linked genes on the inactive X across multiple tissues. Notably, overdosage of Usp9x promotes centrosome ampliﬁcation and chromosome instability, increasing the propensity of tumorigenesis. We further demonstrate that Usp9x overdosage leads to abnormalities in asymmetric cell division, thereby affecting the process of cell differentiation. Thus, Xist repeat B is necessary for gene-speciﬁc silencing during XCI maintenance and impacts cell proliferation and differentiation during development. This provides insights into repeat B importance in maintaining XCI.

Published in

Deletion of Xist repeat B disrupts cell cycle and asymmetric cell division through Usp9x hyperactivation in mice

Liang M, Zhang L, Gong H et al. · Nucleic acids research 2025 · PMID 40042815 · doi:10.1093/nar/gkaf142

This dataset

Open GSE278344 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 GSE278344_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 PRJNA1166688 and SRA study SRP535495. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40042815) ↗

Study design

8 conditions, mostly in triplicate

ATAC-B ×3 ATAC-WT ×3 H2Aub1-B ×3 H2Aub1-WT ×3 Input-B ×3 Input-WT ×3 K27me3-B ×3 K27me3-WT ×2

Supports a between-group comparison across 23 samples.

How we read this: 8 replicated groups read from 23 sample titles; they account for 23 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

GSM8545134 ATAC-B_rep1 ATAC-B
GSM8545135 ATAC-B_rep2 ATAC-B
GSM8545136 ATAC-B_rep3 ATAC-B
GSM8545137 ATAC-WT_rep1 ATAC-WT
GSM8545138 ATAC-WT_rep2 ATAC-WT
GSM8545139 ATAC-WT_rep3 ATAC-WT
GSM8545140 H2Aub1-B_rep1 H2Aub1-B
GSM8545141 H2Aub1-B_rep2 H2Aub1-B
GSM8545142 H2Aub1-B_rep3 H2Aub1-B
GSM8545143 H2Aub1-WT_rep1 H2Aub1-WT
GSM8545144 H2Aub1-WT_rep2 H2Aub1-WT
GSM8545145 H2Aub1-WT_rep3 H2Aub1-WT
GSM8545146 Input-B_rep1 Input-B
GSM8545147 Input-B_rep2 Input-B
GSM8545148 Input-B_rep3 Input-B
GSM8545149 Input-WT_rep1 Input-WT
GSM8545150 Input-WT_rep2 Input-WT
GSM8545151 Input-WT_rep3 Input-WT
GSM8545152 K27me3-B_rep1 K27me3-B
GSM8545153 K27me3-B_rep2 K27me3-B
GSM8545154 K27me3-B_rep3 K27me3-B
GSM8545155 K27me3-WT_rep1 K27me3-WT
GSM8545156 K27me3-WT_rep2 K27me3-WT

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GSE270581 Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq] 24 samples shares deletion

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