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The NuRD chromatin remodeling complex regulates tRNA genes through direct interactions with RNA polymerase III

GSE310006 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 54 samples Submitted 2026/07/09 Platform GPL34281
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 54 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
54 samples: 25 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.
Summary (written by the submitters)
RNA polymerase III (Pol III) synthesizes noncoding RNAs essential for translation, RNA processing, and transcription regulation. Its activity aligns with cellular growth and nutrient availability, and its dysregulation is linked to diseases like breast cancer and leukodystrophy. Despite its importance, Pol III regulators remain largely unidentified due to a lack of exploration of Pol III-centered protein-protein interactions (PPIs).
Read the full summary ↓
To address this need, we conducted high throughput proteomic experiments and identified over 300 novel Pol III interactors, including Pol II-related transcription factors, nuclear import factors, and splicing factors. Most notably, our proteomic survey uncovers complex-complex interactions between Pol III and the NuRD (Nucleosome Remodeling and Deacetylase) complex. NuRD complex is a known Pol II co-repressor, but its recruitment to and effect on Pol III remains uncharacterized. Using innovative large-scale NuRD binding pattern meta-study, NuRD ChIP-seq combined with Pol III inhibition, and Pol III activity profiling in mammalian cell lines, we revealed that the NuRD is recruited by Pol III itself and fine-tunes Pol III transcription activity. We found that NuRD exhibits a binding preference for highly active Pol III genes, and inhibition of Pol III transcription reduced the enrichment of NuRD subunits. Functionally, inhibiting NuRD deacetylase activity releases its inhibition on Pol III transcription and increases its dynamic range. In addition, our ATAC-seq analysis suggests NuRD is potentially involved in establishing nucleosome positioning through its ATP-dependent remodeler activity. Beyond identifying NuRD as a novel Pol III regulator, our survey of Pol III interactions unexpectedly identifies physical interactions between Pol III and mRNA splicing factors. We demonstrate that Pol III depletion leads to rewiring of splicing efficiencies for specific mRNA subpopulations, suggesting a previously unrecognized interplay between Pol III and RNA processing factors. Together, these findings advance our understanding of Pol III interactome, uncovering new layers of transcriptional control and unexpected functional consequences of Pol III interactions in human cells.
This dataset
Open GSE310006 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 GSE310006_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 PRJNA1364997 and SRA study SRP646342. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
25 conditions, mostly in duplicate
THP1,DMSO 2h, biol ×3 THP1,Romidepsin 2h, biol ×3 THP1, 2h,DMSO,sRNA, biol ×3 THP1, 2h,Romidepsin50nM,sRNA, biol ×3 MTA3,THP1,PMA, biol ×2 MTA3,THP1,ML6, biol ×2 MTA3,THP1, biol ×2 MTA2,THP1,PMA, biol ×2 +17 more

Supports a between-group comparison across 54 samples.

How we read this: 25 replicated groups read from 54 sample titles; they account for 54 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

+ 14 more — browse all 54 samples with per-sample file links →

Datasets on a similar topic

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