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PP1 PNUTS binds the “restrictor” and dephosphorylates pol II CTD Ser5 to stimulate RNA pol II transcription termination [ChIP-seq]

GSE269359 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 22 samples Submitted 2025/04/05 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 22 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
22 samples: 6 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.
Paper
PP1/PNUTS phosphatase binds the restrictor complex and stimulates RNA Pol II transcription terminationCell reports · 2025
Summary (written by the submitters)
The restrictor complex, WDR82/ZC3H4, is the major termination factor for antisense transcription from bidirectional promoters, but its mechanism of action is poorly understood. We report that the PP1 phosphatase nuclear targeting subunit PNUTS binds to restrictor via its WDR82 subunit. AlphaFold predicts a quaternary complex, PPWZ, in which PP1-associated PNUTS and ZC3H4 both contact WDR82.
Read the full summary ↓
A chimera comprising inactive PP1H66K fused to the C-terminal PNUTS sequences including its WDR82 binding domain binds to restrictor and acts as a dominant negative inhibitor of antisense termination and CTD Ser5 dephosphorylation. The PP1H66K-PNUTS is a substrate trap that also interacts with pol II large subunit and nuclear exosome components. Ser5 hyperphosphorylated pol II has increased processivity and pauses less frequently than total pol II. We speculate that the elevated elongation efficiency of Ser5-P pol II antagonizes early termination and that Ser5 dephosphorylation by PP1/PNUTS/WDR82/ZC3H4 is coupled to termination of antisense transcription.
Published in
PP1/PNUTS phosphatase binds the restrictor complex and stimulates RNA Pol II transcription termination
Erickson B, Fedoryshchak R, Fong N et al. · Cell reports 2025 · PMID 40244850 · doi:10.1016/j.celrep.2025.115564
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 GSE269359_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 PRJNA1121275 and SRA study SRP512449. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in triplicate
HEK293 PP1(H66K)-PNUTS_mdox_Ser5 ChIPSeq ×3 HEK293 PP1(H66K)-PNUTS_pdox_Ser5 ChIPSeq ×3 HEK293 PP1(H66K)-PNUTSDWBD_mdox_Ser5 ChIPSeq ×3 HEK293 PP1(H66K)-PNUTSDWBD_pdox_Ser5 ChIPSeq ×3 HEK293 PP1(H66K)-PNUTS_mDox_pol II_ChIPseq ×2 HEK293 PP1(H66K)-PNUTS_pDox_pol II_ChIPseq ×2 HEK293 PP1(H66K)-PNUTS_pdox_Avitag ChIPSeq ×1 HEK293 PP1(WT)-PNUTS_pdox_Avitag ChIPSeq ×1 +4 more

Supports a between-group comparison across 16 samples.

How we read this: 6 replicated groups read from 22 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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