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Genome binding/occupancy profiling of USF2 under glucose starvation and changes in H3K27ac based on the presence of USF2

GSE252310 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2024/08/06 Platform GPL21103
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: 2 × USF2 ChIP-seq, Normal, vs 2 × USF2 ChIP-seq, Glucose starvation, vs 2 × Input, Normal, vs 2 × Input, Glucose starvation,Groups 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
USF2 and TFEB compete in regulating lysosomal and autophagy genesNature communications · 2024
Summary (written by the submitters)
Intricate regulation of lysosome and autophagy processes is essential for maintaining cellular homeostasis and basal metabolism. While the consequences of disrupting or attenuating lysosome and autophagy systems have been extensively studied, little is known about the impact of hyper-activation of lysosomal and autophagy genes on homeostasis.
Read the full summary ↓
Our research uncovers previously unknown transcriptional repression mechanism by upstream stimulatory factor 2 (USF2), which inhibits lysosomal and autophagy genes in nutrient-rich conditions. USF2 binds to the CLEAR motif within lysosomal genes along with HDAC1, which diminishes H3K27 acetylation levels, restrains chromatin accessibility, and lowers lysosomal gene expression. Under starvation, USF2 competes with TFEB, a master transcriptional activator of lysosomal and autophagy genes, to bind target gene promoters in phosphorylation-dependent manner. Phosphorylation of the S155 site by GSK3b plays a pivotal role in controlling USF2's DNA binding activity for the repression of lysosomal genes while GSK3b-mediated phosphorylation of TFEB enhances its cytoplasmic retention. Applying these discoveries has potential for treating diseases associated with protein aggregation, including alpha-1 antitrypsin deficiency. These findings demonstrate that the USF2 repression mechanism could be a potent therapeutic strategy for various lysosome and autophagy-related diseases.
Published in
USF2 and TFEB compete in regulating lysosomal and autophagy genes
Kim J, Yu YS, Choi Y et al. · Nature communications 2024 · PMID 39333072 · doi:10.1038/s41467-024-52600-2
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 GSE252310_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 PRJNA1059622 and SRA study SRP480812. Searching any of these in the dataset finder brings you back here.

Study design
2 × USF2 ChIP-seq, Normal, vs 2 × USF2 ChIP-seq, Glucose starvation, vs 2 × Input, Normal, vs 2 × Input, Glucose starvation,

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 8 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
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