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MED26-mediated phase separation regulates erythropoiesis by tuning transcription pausing

GSE212374 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 19 samples Submitted 2025/08/26 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 19 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
19 samples: 17 distinct titles, 2 of them repeatedGroups 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)
The Mediator complex plays a pivotal role in various aspects of transcription and development. However, it remains unclear whether individual Mediator subunits play differential roles during the progression of the developmental process. In this study, we found that the protein level of MED26, a subunit in the core Mediator complex, remained relatively abundant in terminal erythropoiesis, while that of most Mediator subunits drastically diminished.
Read the full summary ↓
MED26 exhibits pronounced phase separation capability, which is essential for erythroid differentiation of primary human erythroblasts. Interestingly, we found that ~60% of chromatin sites with MED26 or MED1 occupancy did not co-localize. Moreover, MED26-enriched loci were associated with RNA polymerase II pausing, and MED26 preferentially interacted with transcription pausing factors, including PAF1, via its TFIIS domain. During erythropoiesis, both the relative abundance of MED26 and the Pausing Index (PI) increased. Erythroid differentiation was promoted by small molecule-induced PI elevation or overexpression of MED26—full-length or the IDR alone—indicating that MED26-associated pausing is necessary for erythropoiesis. In conclusion, this study revealed that MED26 tunes transcription pausing to facilitate erythroid development via a phase separation mechanism.
This dataset
Open GSE212374 in finder → Find more human RNA-seq 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 GSE212374_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 PRJNA875137 and SRA study SRP394937. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
17 distinct titles, 2 of them repeated
K562_WT ×2 K562_MED26_KO ×2

How we read this: Read from 19 sample titles: 17 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
Datasets on a similar topic

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