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A genome-wide screen reveals Ints7 deficiency activates endogenous retrovirus MERVL, accompanied by anastasis of embryonic stem cells [E14TG2a]

GSE293177 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/07/29 Platform GPL13112
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 16 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
16 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
Ints7 deficiency activates DNA damage response to elicit resurgence of endogenous retrovirus MERVL and anastasis of embryonic stem cellsNucleic acids research · 2025
Summary (written by the submitters)
The murine endogenous retrovirus MERVL is closely associated with the developmental potential of totipotency, manifesting dynamic and reversible activation within a small population of in vitro-cultured mouse embryonic stem cells (mESCs). While numerous regulators have been identified to influence the on and off switches of MERVL, how its activation is linked to the cellular decision-making of mESCs remains poorly understood.
Read the full summary ↓
In this study, our genome-wide knockout screen uncovered an intimate relationship between MERVL activation and DNA damage response pathways. Specifically, we found that deficiency of Ints7, a backbone subunit of the Integrator complex, resulted in increased DNA damage, stabilization of p53, and hence transcriptional activation of MERVL. Moreover, we revealed that MERVL activation upon Ints7 knockdown was frequently accompanied by the activation of caspase 3. Intriguingly, a proportion of the caspase-activated mESCs were able to switch on MERVL meanwhile circumvent apoptosis and evade cell death, resembling a process known as anastasis. Altogether, our study highlights an association between MERVL activation and the p53-dependent cell fate plasticity in response to DNA damage, suggesting that limited caspase activation can alter developmental potential of stem cells.
Published in
Ints7 deficiency activates DNA damage response to elicit resurgence of endogenous retrovirus MERVL and anastasis of embryonic stem cells
Shen Y, Li L, Ni H et al. · Nucleic acids research 2025 · PMID 40842237 · doi:10.1093/nar/gkaf797
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 GSE293177_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 PRJNA1243304 and SRA study SRP573859. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 16 more — browse all 16 samples with per-sample file links →

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