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METTL3 Promotes Histone H3K9 Acetylation through Recruitment of Histone Acetyltransferase 1 to Chromatin II

GSE273493 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 10 samples Submitted 2025/12/31 Platform GPL30209
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 10 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
Homo sapiens (human)
Samples
10 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.
Summary (written by the submitters)
METTL3 constitutes the catalytic subunit of the major methyltransferase complex mediating the formation of N6-methyladenosine (m6A) in mRNA. Although the resulting m6A is known to regulate numerous cellular processes, the protein interaction network of this complex remains largely unknown. Here, we employed ascorbate peroxidase-based proximity labeling followed by LC-MS/MS analysis to examine systematically the interaction proteins of METTL3 and METTL14 in HEK293T cells.
Read the full summary ↓
Aside from many proteins involved in mRNA splicing, a subset of histone regulatory proteins are enriched in the proximity proteome of METTL3, including histone acetyltransferase 1 (HAT1). In addition, genetic ablation of METTL3 led to reduced chromatin occupancy of HAT1 isoform-a, which is expressed exclusively in the nucleus, and diminished H3K9Ac in HEK293T cells, especially in retrotransposons. Depletion of HAT1 led to diminished H3K9Ac, which could be restored by wild-type HAT but not the one fused with the nuclear export sequence (NES) of PKI to remove it from the nucleus. Our in vitro acetylation assay further confirmed the acetylation activity of HAT1 isoform-a on nucleosome histone H3K9. The reduced retrotransposons H3K9Ac in METTL3-/- cells could be restored by ectopic expression of wild-type METTL3, but not its catalytically inactive D395A mutant. Together, we assessed the protein interactome of METTL3, uncovered a new function of HAT1 in acetylating H3K9 in chromatin, and revealed a crosstalk between METTL3-mediated formation of m6A and HAT1-catalyzed formation of H3K9Ac in chromatin.
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 GSE273493_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 PRJNA1142007 and SRA study SRP523144. Searching any of these in the dataset finder brings you back here.

Samples in this study

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