GEO series

KMT2D-Mediated H3K4methylation is Essential for GATA1 Transcriptional Activation in Erythropoiesis [ChIP-seq]

GSE293474 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2026/04/10 Platform GPL18460

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 24 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: 24 samples: 24 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; 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 regulation of enhancer activity is essential for cell differentiation and different diseases. KMT2D is considered a significant histone methyltransferase that catalyzes H3K4me1 on enhancers and activates the enhancers by recruiting acetyltransferase for H3K27ace. However, how exactly enhancer activation is determined in human erythropoiesis remains incompletely understood.

Read the full summary ↓

Here, by using an unbiased genetic screen in human erythroblasts, we identified and verified that KMT2D is an essential factor for human erythropoiesis. Accordingly, we observed that KMT2D is indispensable for the activation of erythroid signature genes. Moreover, to further study the direct transcriptional regulatory role of KMT2D, we employed the auxin-inducible degron 2 (AID2) system in human erythroblast cell lines to systematically investigate the effects of acute depletion of KMT2D on transcriptional programs, the genome-wide occupancy of KMT2D and the erythroid master regulator GATA1. Importantly, we revealed that KMT2D colocalized with GATA1 on more than one thousand active enhancers. Moreover, the GATA1 and KMT2D co-localized enhancers exhibit significant higher activities relative to the GATA1 only occupied enhancers. After the depletion of KMT2D, the active histone marks on those enhancers were significantly reduced in accompanying with suppression of the selective targets of GATA1, including numerous erythroid genes (such as ZFPM1, SLC4A1, and EPOR). These results suggest that KMT2D is indispensable for the activation of erythroid gene expression by GATA1. Thus, our results revealed a novel role of KMT2D in the selective dependency of GATA1 on active enhancers, which could impact the transcriptional regulation of KMT2D in both hematopoiesis and blood cancers.

This dataset

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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 GSE293474_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 PRJNA1244765 and SRA study SRP575783. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

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

Supports a case/control comparison: 3 samples read as cases, 1 as controls.

How we read this: Read from 24 sample titles: 24 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

GSM8883058 HUDEP2 cells; DMSO treated_rep1;KMT2D;ChIP-seq
GSM8883059 HUDEP2 cells; DMSO treated_rep2;KMT2D;ChIP-seq
GSM8883060 HUDEP2 cells; DMSO treated_rep3;KMT2D;ChIP-seq
GSM8883061 HUDEP2 cells; 5-Ph-IAA treated_rep1;KMT2D;ChIP-seq
GSM8883062 HUDEP2 cells; 5-Ph-IAA treated_rep2;KMT2D;ChIP-seq
GSM8883063 HUDEP2 cells; 5-Ph-IAA treated_rep3;KMT2D;ChIP-seq
GSM8883064 HUDEP2 cells; DMSO_rep1_Input
GSM8883065 HUDEP2 cells; 5-Ph-IAA_rep1_Input
GSM8883066 HUDEP2 cells; NT_rep1;H3K4me1;ChIP-seq
GSM8883067 HUDEP2 cells; KO_rep1;H3K4me1;ChIP-seq
GSM8883068 HUDEP2 cells; NT_rep2;H3K4me1;ChIP-seq
GSM8883069 HUDEP2 cells; KO_rep2;H3K4me1;ChIP-seq
GSM8883078 HUDEP2 cells; NT_rep1;H3K27ac;ChIP-seq
GSM8883079 HUDEP2 cells; KO_rep1;H3K27ac;ChIP-seq
GSM8883080 HUDEP2 cells; NT_rep2;H3K27ac;ChIP-seq
GSM8883081 HUDEP2 cells; KO_rep2;H3K27ac;ChIP-seq
GSM8883084 HUDEP2 cells; NT_rep1;GATA1;ChIP-seq
GSM8883085 HUDEP2 cells; KO_rep1;GATA1;ChIP-seq
GSM8883086 HUDEP2 cells; NT_rep2;GATA1;ChIP-seq
GSM8883087 HUDEP2 cells; KO_rep2;GATA1;ChIP-seq
GSM8883090 HUDEP2 cells;NT_rep1_Input
GSM8883091 HUDEP2 cells;KO_rep1_Input
GSM8883092 HUDEP2 cells;NT_rep2_Input
GSM8883093 HUDEP2 cells;KO_rep2_Input

Datasets on a similar topic

GSE281735 CTCF is selectively required for maintaining chromatin accessibility and gene expression in human erythropoiesis [ChIP-seq_GATA1] 8 samples shares gata1, erythropoiesis, chip-seq
GSE319078 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers 4 samples shares gata1, essential
GSE309721 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers [ATAC-seq] 4 samples shares gata1, essential
GSE319244 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers [CUT&RUN] 2 samples shares gata1, essential
GSE293567 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers 67 samples shares gata1, essential
GSE275664 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers 16 samples shares gata1, essential
GSE319075 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers [GATA1 RNA-Seq] 9 samples shares gata1, essential
GSE319076 The H3K4 methyltransferase KMT2D is an essential cofactor for GATA1 at erythroid gene enhancers [washout RNA-seq] 8 samples shares gata1, essential

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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.