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SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain

GSE261744 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2024/11/15 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 24 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
24 samples: 8 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
SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor DomainNucleic acids research · 2024
Summary (written by the submitters)
SETDB1 is a major H3K9 methyltransferase. It contains a unique Triple Tudor Domain (3TD) which specifically bind the dual modification of H3K14ac in the presence of H3K9me1/2/3. In this study, we explored the role of the 3TD H3K14ac interaction in the H3K9 methylation activity by SETDB1. We generated the 3TD binding reduced F332A mutant and demonstrate in biochemical methylation assays on recombinant nucleosomes containing H3K14ac analogs, that H3K14 acetylation is crucial for the 3TD mediated recruitment of SETDB1.
Read the full summary ↓
We also see this effect in the cells where SETDB1 binding and activity was globally correlated with H3K14ac, and knock-out (KO) of the H3K14 acetyltransferase HBO1 caused a drastic reduction in the H3K9me3 levels at SETDB1 dependent sites. Further analyses revealed that 3TD was not required for SETDB1 recruitment for regions targeted by KAP1, but at specific target regions, SETDB1 KO could not be efficiently reconstituted by a 3TD mutant of SETDB1 as shown by the finding that H3K9 methylation of L1M repeat elements is highly dependent on an intact 3TD. In summary, our data demonstrate an important role of the 3TD interaction with H3 tails containing K14ac and K9 methylation in the recruitment of SETDB1 to chromatin which is particularly relevant at L1M repeats.
Published in
SETDB1 activity is globally directed by H3K14 acetylation via its Triple Tudor Domain
Chandrasekaran TT, Choudalakis M, Bröhm A et al. · Nucleic acids research 2024 · PMID 39540436 · doi:10.1093/nar/gkae1053
This dataset
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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 GSE261744_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1088534 and SRA study SRP495520. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39540436) ↗
Study design
8 conditions, mostly in duplicate
HCT116_WT_H3K9me3 ×2 HCT116_SETDB1_KO_H3K9me3 ×2 HCT116_SETDB1_H1224K_H3K9me3 ×2 HCT116_SETDB1_WT_H3K9me3 ×2 HCT116_SETDB1_F332A_H3K9me3 ×2 HCT116_HBO1_KO_H3K9me3 ×2 HCT116_WT_H3K14ac ×2 HCT116_SETDB1_KO_H3K14ac ×2 +8 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 24 sample titles; they account for 16 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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