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The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers [CUT&RUN]

GSE319244 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 2 samples Submitted 2026/04/10 Platform GPL18460
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 2 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
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)
By using an unbiased genetic screen and proteome profiling in human erythroblast, we identified and verified KMT2D as an essential factor for human erythropoiesis. Accordingly, we observed that KMT2D is indispensable for the activation of erythroid signature genes in a stage dependent manner.
Read the full summary ↓
Moreover, to further study the direct transcriptional regulatory role of KMT2D, we established two endogenous N-terminus AID-KMT2D system in t human erythroblast cell lines and systematically investigated the effects of acute KMT2D loss by auxin-inducible degron system on transcriptional programs and chromatin accessibility. By integrating multi-omics datasets, we revealed that acute KMT2D loss notably suppressed the subset of GATA1 downstream targets. Importantly, we profiled the specific genome-wide occupancy of KMT2D by comparison between the presence and absence of KMT2D in AID model. Strikingly, KMT2D occupies over hundreds of erythroid specific genes mostly on their promoters. More importantly, we revealed that the KMT2D co-localized with GATA1 in numerous erythroid genes and the occupancy of GATA1 significantly reduced after KMT2D degradation. These results suggest KMT2D is indispensable for the enhancer-binding of GATA1 in gene expression in erythroid lineage specification.
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 GSE319244_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 PRJNA1422666 and SRA study SRP676481. Searching any of these in the dataset finder brings you back here.

Samples in this study

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