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MED16 negatively regulates erythropoiesis and myelopoiesis through modulation of chromatin accessibility [scRNA-Seq]

GSE248810 Homo sapiens (human) Single-cell RNA-seq 2 samples Submitted 2025/01/01 Platform GPL20795
At a glance

Single-cell RNA-seq · human · 2 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism
Homo sapiens (human)
Topic
Myelodysplastic syndromesThis series is part of our curated briefing on it.
Samples
2 samples
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 crucial role in regulating gene expression by interacting with transcription factors. In this study, we investigated the function of MED16, a core member of the tail module of the Mediator complex, in hematopoietic development. Our findings reveal that MED16 serves as a critical modulator of hematopoiesis by controlling chromatin accessibility at specific target genes.
Read the full summary ↓
Loss of MED16 leads to a shift towards erythropoiesis and myelopoiesis in both human and mouse models. We found that MED16 deficiency increases chromatin accessibility at the RUNX1-binding promoter, promoting the expression of erythroid and innate immunity genes through cooperation with the FAcilitate Chromatin Transcription (FACT) complex. Furthermore, our study suggests that high MED16 expression may serve as a potential biomarker for myelodysplastic syndromes (MDS). Knockdown of MED16 in bone marrow mononuclear cells (BMMNCs) of MDS promotes erythroid differentiation, which may offer a potential therapeutic strategy for hematopoietic dysplasia diseases. Our findings demonstrate that MED16 acts as a negative regulator of erythroid and myeloid development and demonstrate its critical role in modulating the chromatin landscape in cooperation with RUNX1 and the FACT complex.
This dataset
Open GSE248810 in finder → Find more human RNA-seq datasets → Myelodysplastic syndromes landscape →
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 GSE248810_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1046051 and SRA study SRP474768. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Samples in this study

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