GEO series

Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming [ES_ChIP_seq_H3K9ac_H3K27ac_LA]

GSE278999 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2025/11/20 Platform GPL23479

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 24 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: 24 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: Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogrammingNature metabolism · 2026

Summary (written by the submitters)

Spatiotemporal changes in the nuclear lamina and cell metabolism shape cell fate, yet their interplay is poorly understood. Here, we identify lamin A/C as a key regulator of cysteine catabolic flux essential for proper cell fate and longevity. Its loss in naïve mouse pluripotent stem cells leads to upregulation of the cysteine generating and catabolizing enzymes, cystathionine γ-lyase (CTH) and cystathionine β-synthase (CBS), thereby promoting de novo cysteine synthesis.

Read the full summary ↓

Increased cysteine flux into acetyl-CoA fosters histone H3K9 and H3K27 acetylation, triggering a transition from naïve to primed pluripotency and abnormal cell fate and function. Conversely, the toxic gain-of-function mutation of Lmna, encoding lamin A/C and associated with premature aging, reduces CTH and CBS levels. This reroutes cysteine catabolic flux and alters the balance between H3K9 acetylation and methylation, crucially impacting germ layer formation and genome stability. Importantly, modulation of Cth and Cbs rescues the abnormal cell fate and function, restores the DNA damage repair capacity, and alleviates the senescent phenotype caused by lamin A/C mutations, highlighting the potential of modulating cell metabolism to mitigate epigenetic diseases.

Published in

Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming

Wang Y, Shi H, Wittig J et al. · Nature metabolism 2026 · PMID 41606307 · doi:10.1038/s42255-025-01443-2

This dataset

Open GSE278999 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 GSE278999_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 PRJNA1169894 and SRA study SRP537340. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41606307) ↗

Samples in this study

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+ 24 more — browse all 24 samples with per-sample file links →

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