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PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression [ChIP-seq]

GSE180483 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 88 samples Submitted 2024/06/07 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 88 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
88 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
PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progressionNature communications · 2024
Summary (written by the submitters)
Genes encoding subunits of SWI/SNF chromatin remodeling complexes are mutated in nearly 25% of cancers. The SWI/SNF subunit SMARCB1 is the driving mutation in nearly all cases of rhabdoid tumor (RT), highly malignant cancers of childhood. While loss of SMARCB1 drives cancer, its absence also creates unique dependencies, which can illuminate mechanism and reveal potential therapeutic vulnerabilities.
Read the full summary ↓
To identify such dependencies we undertook a genome-scale CRISPR screen comparing RT cell lines to 800 other cancer lines. We identified PHF6 as specifically essential for RT cell survival. Germline mutations in both SMARCB1 and PHF6 cause Coffin-Siris syndrome, and somatic mutations in PHF6 or SWI/SNF occur in T-ALL, suggesting a mechanistic link. We establish that PHF6 co-localizes with residual SWI/SNF complexes at active promoters and enhancers. We find that PHF6 is specifically required for H3K14ac accumulation immediately downstream of active promoters and for release of paused Pol II. Collectively, our work identifies novel integrated roles for PHF6 in chromatin and Pol II regulation, establishes a mechanistic basis for dependence upon PHF6 in RT, and reveals a novel potential therapeutic vulnerability in RT.
Published in
PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression
Mittal P, Myers JA, Carter RD et al. · Nature communications 2024 · PMID 39181868 · doi:10.1038/s41467-024-51566-5
This dataset
Open GSE180483 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →
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 GSE180483_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 PRJNA748396 and SRA study SRP329128. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39181868) ↗
Study design
19 conditions, mostly in duplicate
G401_shPHF6_H3K27ac ×3 G401_shCTRL_H3K27ac ×3 G401_shCTRL_H3K36me2 ×3 G401_shCTRL_H3K4me1 ×3 G401_shPHF6_H3K4me1 ×3 G401_shPHF6_H3K4me3 ×3 G401_shCTRL_POLII ×2 G401_shPHF6_POLII ×2 +55 more

Supports a between-group comparison across 44 samples.

How we read this: 19 replicated groups read from 88 sample titles; they account for 44 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

+ 48 more — browse all 88 samples with per-sample file links →

Datasets on a similar topic

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