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CDK7 kinase activity promotes RNA polymerase II promoter escape by facilitating initiation factor release

GSE218269 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 100 samples Submitted 2024/06/01 Platform GPL21697
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 100 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
100 samples: 40 conditions, mostly in triplicateGroups 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.
Summary (written by the submitters)
Cyclin-dependent kinase 7 (CDK7), part of general transcription factor TFIIH, promotes gene transcription by phosphorylating the C-terminal domain of RNA polymerase II (Pol II). Here, we combine rapid CDK7 kinase inhibition with multi-omics analysis to unravel the direct functions of CDK7 in human cells. CDK7 inhibition causes Pol II retention at promoters, leading to decreased Pol II initiation and immediate global downregulation of transcript synthesis.
Read the full summary ↓
Elongation, termination, and recruitment of co-transcriptional factors are not directly affected. Although Pol II, initiation factors, and Mediator accumulate at promoters, Pol II complexes can also proceed into gene bodies without promoter-proximal pausing while retaining initiation factors and Mediator. Further downstream, Pol II phosphorylation increases, initiation factors and Mediator are released, allowing recruitment of elongation factors and increase in Pol II elongation velocity. Collectively, CDK7 kinase activity promotes the release of initiation factors and Mediator from Pol II, facilitating Pol II escape from the promoter.
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 GSE218269_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 PRJNA902829 and SRA study SRP408495. Searching any of these in the dataset finder brings you back here.

Study design
40 conditions, mostly in triplicate
HEK293CDK7as_MNaseChIPseq_PolII_RPB1_DMSO_30m… ×3 HEK293CDK7as_MNaseChIPseq_PolII_RPB1_1-NM-PP1… ×3 HEK293CDK7as_MNaseChIPseq_Ser5P_CTD_RPB1_DMSO… ×3 HEK293CDK7as_MNaseChIPseq_Ser5P_CTD_RPB1_1-NM… ×3 HEK293CDK7as_MNaseChIPseq_MED26_DMSO_30min ×3 HEK293CDK7as_MNaseChIPseq_MED26_1-NM-PP1_30min ×3 HEK293CDK7as_MNaseChIPseq_TFIIB_DMSO_30min ×3 HEK293CDK7as_MNaseChIPseq_TFIIB_1-NM-PP1_30min ×3 +32 more

Supports a between-group comparison across 100 samples.

How we read this: 40 replicated groups read from 100 sample titles; they account for 100 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

+ 60 more — browse all 100 samples with per-sample file links →

Datasets on a similar topic

Search all human RNA-seq datasets in GEO →

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