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Transcriptomic reprogramming driven by nuclear and cell size perturbations via compartment-specific protein accumulation and G1 arrest in yeast and human cells

GSE339383 Saccharomyces cerevisiae (yeast) ChIP-seq / ATAC-seq (genome binding and open chromatin) 107 samples Submitted 2026/07/23 Platform GPL34284Platform GPL34739
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · yeast · 107 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
Saccharomyces cerevisiae (yeast)
Samples
107 samples: 35 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)
While nuclear and cell sizes are critical determinants of cellular function, their specific impacts on gene expression remain poorly understood. To dissect the direct transcriptomic consequences of nuclear size alterations, we engineered inducible systems in budding yeast (Saccharomyces cerevisiae) that accumulate massive proteins specifically within the nucleus (3xFP-NLS) or the cytosol (3xFP-NES), alongside corresponding control systems (empty vector, 3xFP, and 1xFP-NLS).
Read the full summary ↓
Using these systems, we profiled global transcript abundance and RNA polymerase II (Pol II) occupancy via high-throughput mRNA-seq and ChIP-seq. Furthermore, to uncouple the transcriptomic effects of general cell volume expansion from nuclear size changes, we performed mRNA-seq on a temperature-sensitive G1-arrest yeast mutant (cdc28-13) expressing the cytosolic accumulation system (3xFP-NES) under restricted temperature (37°C). Finally, to examine the evolutionarily conserved impact of excessive cell expansion in mammalian systems, we performed mRNA-seq on human retinal pigment epithelial (RPE1) cells undergoing palbociclib-induced G1 arrest over an extended time course. Collectively, our integrated cross-species multi-omics analyses uncover a fundamental, nuclear size-dependent transcriptome reprogramming mechanism.
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 GSE339383_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 PRJNA1498557 and SRA study SRP719983. Searching any of these in the dataset finder brings you back here.

Study design
35 conditions, mostly in triplicate
Human RPE1 Day2 ×4 Human RPE1 Day7 ×4 A3xFP-NLS EST ×3 A3xFP-NLS EtOH ×3 Aempty EST ×3 Aempty EtOH ×3 A3xFP-NES EST ×3 A3xFP-NES EtOH ×3 +27 more

Supports a between-group comparison across 107 samples.

How we read this: 35 replicated groups read from 107 sample titles; they account for 107 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

+ 67 more — browse all 107 samples with per-sample file links →

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