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PROSER1 Modulates DNA Demethylation through Dual Mechanisms to Prevent Syndromic Developmental Malformations [RNA-seq]

GSE273516 Mus musculus (mouse) DNA methylation 12 samples Submitted 2024/11/21 Platform GPL24247
At a glance

DNA methylation · mouse · 12 samples

What it is
DNA methylationChemical marks on DNA that help switch genes on or off.
Organism
Mus musculus (mouse)
Samples
12 samples: 6 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
PROSER1 modulates DNA demethylation through dual mechanisms to prevent syndromic developmental malformationsGenes & development · 2024
Summary (written by the submitters)
The link between DNA methylation and neurodevelopmental disorders is well established. However, how DNA methylation is fine-tuned – ensuring precise gene expression and developmental fidelity – remains poorly understood. PROSER1, a known TET2 interactor, was recently linked to a severe neurodevelopmental disorder. Here, we demonstrate that PROSER1 interacts with all TET enzymes and stabilizes chromatin-bound TET-OGT-PROSER1-DBHS (TOPD) complexes, which regulate DNA demethylation and developmental gene expression.
Read the full summary ↓
Surprisingly, we find that PROSER1 also sequesters TET enzymes, preventing widespread demethylation and transposable element de-repression. Our findings identify PROSER1 as a key factor which both positively and negatively regulates DNA demethylation essential for mammalian neurodevelopment.
Published in
PROSER1 modulates DNA demethylation through dual mechanisms to prevent syndromic developmental malformations
Fleming A, Knatko EV, Li X et al. · Genes & development 2024 · PMID 39562138 · doi:10.1101/gad.352176.124
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 GSE273516_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 PRJNA1142189 and SRA study SRP523252. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
wildtype mESC RNA-seq biol ×2 wildtype day2 in N2B27 RNA-seq biol ×2 PROSER1 KO mESC RNA-seq biol ×2 PROSER1 KO day2 in N2B27 RNA-seq biol ×2 PROSER1 KO+Rescue mESC RNA-seq biol ×2 PROSER1 KO+Rescue day2 in N2B27 RNA-seq biol ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 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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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.