← BioTransfer GEO Dataset Finder
GEO series

H2A.Z is required to initiate DNA repair to prevent premature aging

GSE216935 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2024/03/04 Platform GPL21103
Summary
Histone variants are key epigenetic players, but their functional and physiological roles remain poorly understood. Here, we show that depletion of the histone variant H2A.Z in mouse skeletal muscle causes oxidative stress, oxidation of proteins, accumulation of DNA damages, and both neuromuscular junction and mitochondria lesions that consequently lead to premature muscle aging and reduced life span. Investigation of the molecular mechanisms involved shows that H2A.Z is required to initiate DNA double strand break repair by recruiting Ku80 at DNA lesions. This is achieved via specific interactions of Ku80 vWA domain with H2A.Z. Taken as a whole, our data reveal that H2A.Z containing nucleosomes act as a molecular platform to bring together the proteins required to initiate and process DNA double strand break repair.
Published in
H2A.Z is involved in premature aging and DSB repair initiation in muscle fibers
Belotti E, Lacoste N, Iftikhar A et al. · Nucleic acids research 2024 · PMID 38281187 · doi:10.1093/nar/gkae020
This dataset
Download

Direct links to NCBI, no account and no request form: the whole study as GSE216935_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA896205 and SRA study SRP405512. Searching any of these in the dataset finder brings you back here.

Samples in this study

The sample list for this study is not cached yet. Press Sort into groups and it will be fetched from NCBI.

+ 6 more — browse all 6 samples with per-sample file links →

Similar datasets

Search all mouse RNA-seq datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.