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Exploring the Role of DNMT1 in RNA m⁵C Methylation (eCLIPseq II)

GSE290473 Homo sapiens (human) DNA methylation 11 samples Submitted 2025/05/06 Platform GPL24676
At a glance

DNA methylation · human · 11 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Homo sapiens (human)
Samples
11 samples: 5 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.
Paper
DNA methyltransferase 1 modulates mitochondrial function through bridging m(5)C RNA methylationMolecular cell · 2025
Summary (written by the submitters)
DNA methyltransferase 1 (DNMT1) is an enzyme known for DNA methylation maintenance. However, point mutations in its RFTS domain lead to late-onset neurodegeneration such as the autosomal dominant cerebellar ataxia-deafness and narcolepsy (ADCA-DN) disorder. Here we demonstrated that wild-type DNMT1 also has the capability to bind to mRNA transcripts and facilitate 5-methylcytosine (m5C) RNA methylation by recruiting NOP2/Sun RNA methyltransferase 2 (NSUN2).
Read the full summary ↓
RNA m5C methylation, in turn, promotes RNA stability for those genes modulating mitochondrial function. When DNMT1 RFTS domain is mutated in the case of ADCA-DN disorder, it triggers aberrant DNMT1-RNA interaction and significantly elevated m5C RNA methylation and RNA stability for a portion of metabolic genes. Consequently, increased levels of metabolic RNA transcripts contribute to cumulative oxidative stress, mitochondrial dysfunction, and neurological symptoms. Collectively, our results highlight a novel role for DNMT1 in regulating both DNA and RNA methylation as well as mitochondrial function, shedding light on the pathogenic mechanism of DNMT1 mutation-induced neurodegeneration.
Published in
DNA methyltransferase 1 modulates mitochondrial function through bridging m(5)C RNA methylation
Wang J, Deng X, Jian T et al. · Molecular cell 2025 · PMID 40328247 · doi:10.1016/j.molcel.2025.04.019
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 GSE290473_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 beta-value tables or raw IDAT files among the supplementary files.

Also filed as BioProject PRJNA1228131 and SRA study SRP566262. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly in duplicate
eCLIP-seq NSUN2 IP ×2 eCLIP-seq NSUN2 Input ×2 eCLIP-seq DNMT1 IP HeLa ×2 eCLIP-seq DNMT1 Input HeLa ×2 eCLIP-seq DNMT1 IP 293T ×2 eCLIP-seq DNMT1 Input 293T ×1

Supports a between-group comparison across 10 samples.

How we read this: 5 replicated groups read from 11 sample titles; they account for 10 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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