GEO series

PDX1 Phosphorylation Mediates Amino Acid-mTORC1 Signaling in Pancreatic β-Cells [ChIP-seq]

GSE278789 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/12/01 Platform GPL24247

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 16 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: 16 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.
Paper: PDX1 phosphorylation at S61 by mTORC1 links nutrient signaling to β cell function and metabolic diseaseCell reports · 2026

Summary (written by the submitters)

PDX1 is known as the insulin transcription factor that regulates insulin expression in pancreatic β-cells in response to circulating glucose levels. Our previous study showed PDX1 also acts as a downstream effector that mediates β-cell mTORC1 signaling in the control of whole-body glucose homeostasis in response to stimulation by amino acids (AAs).

Read the full summary ↓

Here we report that PDX1 has a broad role in AA-mTORC1-regulated transcriptome in β-cells, especially in processes related to β-cell proliferation and function. Mechanistically, mTORC1 phosphorylates PDX1 at S61 in an AA-dependent and rapamycin-sensitive manner. S61 phosphorylation promotes PDX1 protein levels and transcriptional activity. Interestingly, S61 is located within the transactivation domain targeted by monogenic diabetes mutations, which interfere with S61 phosphorylation and PDX1's transcriptional activity. To help understand the role of S61 phosphorylation in vivo, we generated S61A and S61E genomic mutations in mice, mimicking the unphosphorylated and phosphorylated states, respectively. Our results indicate that S61 phosphorylation positively regulates insulin expression and β-cell proliferation, promoting Western diet-induced hyperinsulinemia, obesity, and liver steatosis. These findings reveal the mechanism and roles of AA-mTORC1-PDX1 signaling in the control of pancreatic β-cell proliferation and function under physiological and pathological conditions.

Published in

PDX1 phosphorylation at S61 by mTORC1 links nutrient signaling to β cell function and metabolic disease

Fan J, Zhang X, Zhang J et al. · Cell reports 2026 · PMID 41528843 · doi:10.1016/j.celrep.2025.116811

This dataset

Open GSE278789 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 GSE278789_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 PRJNA1168924 and SRA study SRP536609. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41528843) ↗

Samples in this study

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+ 16 more — browse all 16 samples with per-sample file links →

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