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Series GSE216935 Query DataSets for GSE216935
Status Public on Mar 04, 2024
Title H2A.Z is required to initiate DNA repair to prevent premature aging
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
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.
 
Overall design To adress the effect of H2A.Z on transcription, we have used skeletal muscles isolated from WT and H2A.Z null 12 months-old animals
 
Contributor(s) Belotti E, Lacoste N, Iftikhar A, Simonet T, Papin C, Streichenberger N, Mari P, Girard E, Osseni A, Giglia-Mari G, Dimitrov S, Hamiche A, Schaeffer L
Citation(s) 38281187
Submission date Oct 31, 2022
Last update date May 01, 2024
Contact name Christophe Papin
E-mail(s) papin@igbmc.fr
Organization name IGBMC - CNRS UMR 7104 - Inserm U 964
Street address 1 rue Laurent Fries
City ILLKIRCH-GRAFFENSTADEN
ZIP/Postal code 67404
Country France
 
Platforms (1)
GPL21103 Illumina HiSeq 4000 (Mus musculus)
Samples (6)
GSM6697984 WT-rep1
GSM6697985 WT-rep2
GSM6697986 WT-rep3
Relations
BioProject PRJNA896205

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Supplementary file Size Download File type/resource
GSE216935_RNA.xlsx 4.8 Mb (ftp)(http) XLSX
SRA Run SelectorHelp
Raw data are available in SRA
Processed data are available on Series record

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