GEO series

The NuRD chromatin remodeling complex regulates tRNA genes through direct interactions with RNA polymerase III [Nuclei run-on (nascent RNA) profiling]

GSE311392 Homo sapiens (human) Other 6 samples Submitted 2026/07/09 Platform GPL34284

At a glance

human · 6 samples

Organism: Homo sapiens (human)
Samples: 6 samples: 6 samples, each with a distinct title — no replicated groupsGroups 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.

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 GSE311392 in finder → Find more human datasets →

Download · which file do I need?

Direct links to NCBI, 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.

All supplementary files ↗

3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE311392_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

Also filed as BioProject PRJNA1369399. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

6 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 6 sample titles: 6 distinct titles with little repetition. 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

GSM9324426 A1_mock_DMSO_1
GSM9324427 A2_mock_DMSO_2
GSM9324428 A3_mock_DMSO_3
GSM9324429 A4_mock_ML6_1
GSM9324430 A5_mock_ML6_2
GSM9324431 A6_mock_ML6_3

Datasets on a similar topic

GSE215328 Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [hESC_H9_d049_ChIP_Seq] 135 samples shares remodeling, chromatin, complex
GSE253694 Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [HEK293T_siNURD_CTCF_ChIP_Seq] 36 samples shares remodeling, chromatin, complex
GSE215326 Pivotal Role of the NuRD Complex in Remodeling Chromatin Environment and Maintaining Genome Architecture at CTCF Sites [HEK293T_IAA72h_ChIP_Seq] 30 samples shares remodeling, chromatin, complex
GSE314625 WSTF deficiency reprograms regulatory networks by linking locus‑specific chromatin remodeling to altered isoform expression and misdirected signaling [mRNA-seq] 18 samples shares remodeling, chromatin, direct
GSE333557 RNA Polymerase III inhinition leads to changes in protein coding gene expression 54 samples shares iii, polymerase
GSE306294 An RNA polymerase III tissue and tumor atlas uncovers context-specific activities linked to 3D epigenome regulatory mechanisms 24 samples shares iii, polymerase
GSE243298 3D Chromatin Remodeling in B-cell Development and B-cell Acute Lymphoblastic Leukemia [Hi-C] 35 samples shares remodeling, chromatin
GSE193413 Super-silencer perturbation by EZH2 and REST inhibition leads to large loss of chromatin interactions and reduction in cancer growth [Hi-C] 28 samples shares interactions, chromatin

Search all human datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.