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Tripartite phosphorylation of SPT5 by CDK9 times pause release and tunes elongation rate of RNA polymerase II (ChIP-Seq)

GSE265881 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 72 samples Submitted 2025/04/17 Platform GPL24676Platform GPL20301
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 72 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
72 samples: 32 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
Tripartite phosphorylation of SPT5 by CDK9 times pause release and tunes elongation rate of RNA polymerase IIMolecular cell · 2025
Summary (written by the submitters)
The RNA polymerase II (RNAPII) transcription cycle is regulated throughout its duration by protein phosphorylation. Previously, two regions phosphorylated by cyclin-dependent kinase 9 (CDK9) in elongation factor SPT5—the linker between Kyrpides-Ouzounis-Woese (KOW) x-4 and 5 domains and carboxy-terminal repeat (CTR) 1—were implicated in promoter-proximal pausing and termination, respectively.
Read the full summary ↓
Here, we show that phosphorylations in the linker, CTR1, and a third region, CTR2, coordinately control pause release, elongation speed, and termination in HCT116 human colon cancer cells. Pausing was unaffected or increased by mutations preventing CTR1 or CTR2 phosphorylation, respectively, but attenuated when both CTRs were mutated. Whereas loss of CTR1 phosphorylation slowed elongation and repressed nascent transcription, simultaneous CTR2 mutation partially reversed both effects. Nevertheless, mutating both CTRs had additive effects on splicing, termination, steady-state mRNA levels, and cell proliferation. Therefore, tripartite SPT5 phosphorylation times pause release and tunes RNAPII elongation rate to ensure productive transcription and cell viability.
Published in
Tripartite phosphorylation of SPT5 by CDK9 times pause release and tunes elongation rate of RNA polymerase II
Sun R, Fisher RP · Molecular cell 2025 · PMID 40250441 · doi:10.1016/j.molcel.2025.03.021
This dataset
Open GSE265881 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 GSE265881_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 PRJNA1104616 and SRA study SRP504053. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40250441) ↗
Study design
32 conditions, mostly in duplicate
dTAG-SPT5-HCT116, dTAGv-1(-), ×2 dTAG-SPT5-HCT116, dTAGv-1(+), ×2 dTAG-SPT5-HCT116, WT, ×2 dTAG-SPT5-HCT116, muR1, ×2 dTAG-SPT5-HCT116, muR2, ×2 dTAG-SPT5-HCT116, muR1R2, ×2 dTAG-SPT5-HCT116, muALL, ×2 dTAG-SPT5-HCT116, WT_∆CTR2, ×2 +32 more

Supports a between-group comparison across 64 samples.

How we read this: 32 replicated groups read from 72 sample titles; they account for 64 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

+ 32 more — browse all 72 samples with per-sample file links →

Datasets on a similar topic

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