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PRMT5 regulates splicing of detained introns from DNA damage repair genes to protect against replication stress.

GSE296394 Homo sapiens (human) RNA-seq (gene expression) 18 samples Submitted 2026/06/19 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 18 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
Homo sapiens (human)
Samples
18 samples: 6 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)
Protein arginine methyltransferase 5 (PRMT5) catalyzes the formation of symmetric dimethyl arginine on a broad range of cellular targets, and PRMT5 inhibitors (PRMT5i) show drastic anti-proliferative effects in preclinical studies. Several models have been proposed to explain and predict sensitivity to PRMT5 inhibition including through p53 activation and DNA damage response regulation.
Read the full summary ↓
Here, we interrogate the underlying mechanisms of PRMT5i sensitivity in Merkel cell carcinoma, a high-grade neuroendocrine carcinoma of the skin that is that is highly sensitive to p53 activation. We observed that although PRMT5 inhibition activated p53, p53 loss did not impact PRMT5i sensitivity. To identify critical pathways altered by PRMT5i, we conducted a genome-wide CRISPR/Cas9 screen and found that PRMT5i-treated cells have an increased dependency on splicing factors. Furthermore, proteomic analysis found that levels of mRNA splicing factors increased after PRMT5i treatment. Characterization of the transcriptome revealed a disruption in mRNA splicing of detained introns in both PRMT5i sensitive and resistant lines. We observed that basal levels of detained introns correlated with PRMT5 inhibitor sensitivity, and that PRMT5 was required to maintain genome integrity through ATR/CHK1 signaling. Our findings support a threshold model of genome stability, in which cells can tolerate an increase in detained introns until a point where DNA damage pathways are triggered, and cells undergo apoptosis.
This dataset
Open GSE296394 in finder → Find more human RNA-seq 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 GSE296394_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: 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 PRJNA1259044 and SRA study SRP583166. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
6 conditions, mostly in triplicate
MKL-1 cells, DMSO treatment, ×3 MKL-1 cells, PRMT5i treatment, ×3 MS-1 cells, DMSO treatment, ×3 MS-1 cells, PRMT5i treatment, ×3 WaGa cells, DMSO treatment, ×3 WaGa cells, PRMT5i treatment, ×3

Supports a between-group comparison across 18 samples.

How we read this: 6 replicated groups read from 18 sample titles; they account for 18 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
Datasets on a similar topic

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