GEO series

CUT&Tag analysis of Isl1CKO and control pancreatic endocrine cells

GSE301940 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 11 samples Submitted 2026/05/14 Platform GPL16417

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 11 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: 11 samples: 11 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.
Paper: ISL1 Restricts Progenitor Programs and Promotes β-Cell Maturation, Revealing Sex Differences in Diabetes ProgressionDiabetes · 2026

Summary (written by the submitters)

Pancreatic endocrine cells regulate glucose homeostasis and energy metabolism in response to nutrients. All endocrine lineages arise from a common progenitor pool through sequential and coordinated cell fate decisions. The homeodomain protein ISL1 functions as a key-lineage determining transcription factor; however, its role in establishing endocrine cell identity and driving terminal maturation remains incompletely characterized.

Read the full summary ↓

By integrating single-cell transcriptomics with H3K27ac and H3K27me3 chromatin profiling, we uncover a reshaped transcriptomic and epigenetic landscape in Isl1-deficient endocrine cells. Loss of Isl1 disrupts α-cell identity, ablates δ- and γ-cell lineages, and results in the persistence of immature, incompletely differentiated β cells in postnatal and adult islets. Longitudinal single-cell profiling revealed that Isl1CKO endocrine cells maintain aberrant differentiation states, exhibit impaired β-cell function, activate diabetes- and stress-associated pathways, and display sex-specific responses linked to disease progression. Mechanistically, ISL1 represses intermediate developmental programs and promotes chromatin remodeling required for terminal differentiation. These findings reveal how interactions between transcription factors and the epigenome coordinate the activation and repression of gene regulatory programs that govern cell fate, and functional maturation in the endocrine pancreas.

Published in

ISL1 Restricts Progenitor Programs and Promotes β-Cell Maturation, Revealing Sex Differences in Diabetes Progression

Fabriciova V, Bohuslavova R, Lebron-Mora L et al. · Diabetes 2026 · PMID 41700921 · doi:10.2337/db25-0673

This dataset

Open GSE301940 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE301940_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 PRJNA1287767 and SRA study SRP598756. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41700921) ↗

Study design

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

Supports a case/control comparison: 4 samples read as cases, 7 as controls.

How we read this: Read from 11 sample titles: 11 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

GSM9092543 endocine pancreas,control1_H3K27me3,1
GSM9092544 endocine pancreas,control2_H3K27me3,1
GSM9092545 endocine pancreas,mutant1_H3K27me3,1
GSM9092546 endocine pancreas,mutant2_H3K27me3,1
GSM9092547 endocine pancreas,control1_H3K27ac,1
GSM9092548 endocine pancreas,control2_H3K27ac,1
GSM9092549 endocine pancreas,mutant1_H3K27ac,1
GSM9092550 endocine pancreas,mutant2_H3K27ac,1
GSM9092551 endocine pancreas,control36_ISL1_E14.5,1
GSM9092552 endocine pancreas,control60_ISL1_E14.5,1
GSM9092553 endocine pancreas,control155_ISL1_P9,1

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