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FTO-Mediated m6A Demethylation Regulates PGC-1α-Dependent Mitochondrial Biogenesis to Attenuate Aluminum-Induced Neuronal Senescence [RNA-Seq]

GSE304247 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/22 Platform GPL21103
Summary
This study employs integrated MeRIP-Seq and RNA-Seq to investigate how aluminum (Al) exposure drives neuronal senescence via m6A methylation dynamics. Triplicate samples of mouse hippocampal neuronal cells (HT22) were analyzed under control conditions and following treatment with aluminum maltolate (Al(mal)₃; 60, 120, 240 μM). Total RNA underwent fragmentation and m6A-specific immunoprecipitation (MeRIP) using m6A antibodies and Dynabeads. Libraries were prepared with the Illumina TruSeq Stranded mRNA Kit and sequenced on the HiSeq X10 platform (paired-end, 150 bp). MeRIP-seq data (aligned to BosGru3.0via HISAT2) revealed Al-induced global hypermethylation (7,068 upregulated m6A peaks, MeTDiff, FDR < 0.05), enriched in coding sequences and annotated to senescence/neurodegeneration pathways (GO/KEGG). RNA-seq identified 6,369 differentially expressed genes (DESeq2, |log₂FC| > 1.5, p < 0.05). Integrative analysis demonstrated coordinated m6A hypermethylation and downregulation of PGC-1αmRNA, linking epitranscriptomic dysregulation to suppressed mitochondrial biogenesis.
Published in
FTO-mediated m6A demethylation regulates PGC-1α-dependent mitochondrial biogenesis to attenuate aluminum-induced neuronal senescence
Jin Z, Li S, Yin J et al. · Scientific reports 2026 · PMID 42098356 · doi:10.1038/s41598-026-51674-w
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Also filed as BioProject PRJNA1299484 and SRA study SRP605611. Searching any of these in the dataset finder brings you back here.

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