GEO series

Circadian entrainment of pancreatic islet function and of the pancreatic islet transcriptome is regulated by glucocorticoid signaling [Multiome]

GSE313095 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 8 samples Submitted 2026/09/28 Platform GPL24247

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 8 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: 8 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)

Glucocorticoid (GC) hormone secretion follows a clear circadian pattern and regulates diverse physiological and molecular functions, including glucose homeostasis. The function of GCs is mediated by the glucocorticoid receptor (GR), a ligand-induced nuclear hormone receptor that promotes expression of genes in a cell-type-specific manner.

Read the full summary ↓

However, the GR cistrome and the corresponding regulatory role of GCs on pancreatic β-cells remain poorly understood. To address these knowledge gaps, we used a combination of transcriptional, epigenetic, and physiological assays to systematically delineate the role of GC signaling in β-cells. Our studies provide the first description of the β-cell GR cistrome demonstrating its enrichment for transcriptional regulators of insulin secretion, β-cell identity, and circadian rhythms. In addition, we also find that GR-dependent β-cell enhancers display circadian expression patterns in vivo and their circadian expression can be amplified and/or phase-shifted by timed administration of synthetic GC in mice. Finally, we also show that restoration of GC signaling in circadian-disrupted mice enhances diurnal glucose tolerance, β-cell function, and circadian rhythmicity of genes enriched for pathways controlling cellular circadian rhythms and insulin secretion. Our findings suggest that the circadian timing of glucocorticoid secretion plays an important role in modulating β-cell circadian gene expression, function and the regulation of glucose tolerance. These findings have direct implications for understanding the physiological role of GCs in the regulation of diurnal glucose homeostasis, and for developing pharmacological approaches using GC therapy.

This dataset

Open GSE313095 in finder → Find more mouse 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 GSE313095_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 PRJNA1378254 and SRA study SRP653947. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 8 more — browse all 8 samples with per-sample file links →

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