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FUS reads histone H3K36me3 to regulate alternative polyadenylation [CUT&Tag]

GSE212423 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 38 samples Submitted 2024/03/21 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 38 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
38 samples: 19 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
FUS reads histone H3K36me3 to regulate alternative polyadenylationNucleic acids research · 2024
Summary (written by the submitters)
Complex organisms are able to generate differential gene expression through the same set of DNA sequences in distinct cells. The communication between chromatin and RNA regulates how cells behave in tissues. However, little is known about how chromatin, especially the histone modifications, regulates RNA polyadenylation. Here, we find that FUS is recruited to chromatin by H3K36me3 at gene bodies.
Read the full summary ↓
Once H3K36me3 is abolished, FUS is dissociated from chromatin to increase the binding with RNA, resulting in increased distal polyadenylation selections that are far from the stop codon. The H3K36me3 recognition of FUS is mediated by the proline residues in ZNF domain, mutations of which lead to reduced chromatin association of FUS, increased RNA binding of FUS, and distal polyadenylation selections. Proline mutation, which corresponds to the mutation in amyotrophic lateral sclerosis, contributes to the hyperactivation of mitochondria and hyperdifferentiation in mouse embryonic stem cells. These findings reveal FUS as an H3K36me3 reader protein that links chromatin-mediated alternative polyadenylation to human disease.
Published in
FUS reads histone H3K36me3 to regulate alternative polyadenylation
Jia J, Fan H, Wan X et al. · Nucleic acids research 2024 · PMID 38499486 · doi:10.1093/nar/gkae184
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 GSE212423_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 PRJNA875408 and SRA study SRP395073. Searching any of these in the dataset finder brings you back here.

Study design
19 conditions, mostly in duplicate
batch1_Fus_Fus_KO1 ×2 batch1_Fus_Fus_KO2 ×2 batch1_Fus_Setd2_KO1 ×2 batch1_Fus_Setd2_KO2 ×2 batch1_Fus_WT ×2 batch1_H3K27me3_Fus_KO1 ×2 batch1_H3K27me3_Fus_KO2 ×2 batch1_H3K27me3_Setd2_KO1 ×2 +11 more

Supports a between-group comparison across 38 samples.

How we read this: 19 replicated groups read from 38 sample titles; they account for 38 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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