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H3K9ac ChIP-seq profiling of wild-type and Slc31a1 conditional knockout mouse bone marrow stromal cells

GSE337269 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2026/07/31 Platform GPL24247
Summary
Age-associated bone loss is largely driven by impaired osteoblast generation from bone marrow stromal cells (BMSCs), but the metabolic and epigenetic mechanisms that regulate osteogenic commitment remain incompletely understood. This study identifies SLC31A1-mediated copper uptake as a cell-intrinsic metabolic checkpoint required for BMSC osteogenic differentiation and skeletal integrity. Mesenchymal lineage-specific Slc31a1 deletion impaired bone formation and BMSC osteogenesis and caused Slc31a1-deficient BMSCs to accumulate in an ID1-high progenitor-like state. To investigate the epigenetic mechanism underlying this phenotype, H3K9ac ChIP-seq was performed in wild-type and Slc31a1 conditional knockout mouse BMSCs. The analysis revealed increased H3K9ac enrichment in Slc31a1-deficient BMSCs, including enhanced H3K9ac signal at the Id1 locus, supporting a model in which SLC31A1-dependent copper uptake maintains mitochondrial complex IV integrity and NAD+ homeostasis to enable SIRT1-dependent epigenetic repression of Id1 during osteogenic commitment.
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Direct links to NCBI, no account and no request form: the whole study as GSE337269_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1484612 and SRA study SRP714392. Searching any of these in the dataset finder brings you back here.

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