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Intrinsically disordered regions restrain genomic targeting of RNA and histone demethylases in mammals and plants [Histone_ALKBH]

GSE286063 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/03/09 Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 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
Mus musculus (mouse)
Samples
12 samples: 6 conditions, mostly in duplicateGroups 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)
Intrinsically disordered regions (IDRs) are well-known facilitators of chromatin regulation, but their role as regulatory restraints remains underexplored. Here, we reveal that the C-terminal IDR of mammalian ALKBH5 anchors its main activity to mRNA, limiting chromatin engagement in mouse embryonic stem cells (mESCs). IDR deletion redirects ALKBH5 to chromatin-associated non-coding RNAs, driving widespread chromatin opening and transcriptional activation.
Read the full summary ↓
This mechanism extends to histone demethylases, where IDR deletion also results in broad removal of repressive histone marks, leading to increased chromatin accessibility and activation of transposable elements. Leveraging these insights, we engineered ALKBH5 and its plant homologs with IDR deletion. Overexpression of these IDR-deleted ALKBH5 demethylases could promote Arabidopsis root growth and increase rice yield. Our findings uncover a conserved role for IDRs in restraining chromatin access by RNA and histone demethylases and establish a new strategy of chromatin programming for crop engineering using plant proteins.
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 GSE286063_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 PRJNA1207566 and SRA study SRP555852. Searching any of these in the dataset finder brings you back here.

Study design
6 conditions, mostly in duplicate
H3K9me3 Alkbh5 del-cIDR ×2 H3K9me3 WT ×2 H3K27ac Alkbh5 del-cIDR ×2 H3K27ac WT ×2 H3K4me3 Alkbh5 del-cIDR ×2 H3K4me3 WT ×2

Supports a between-group comparison across 12 samples.

How we read this: 6 replicated groups read from 12 sample titles; they account for 12 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
Datasets on a similar topic

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