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Knockdown of Histone H1.5 leads to a loss in centromeric transcription

GSE242112 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/01/14 Platform GPL16791
Summary
Mammalian linker histone proteins (Histone H1) comprise a group of 11 non-allelic variants which have key roles in modulating chromatin organization. Subtype specific genomic distribution can contribute to a fine- tuned regulation of gene expression and chromatin architecture. In this study, we report that the variant histone H1.5 localizes to human centromeres and has a functional role in regulation of centromeric noncoding transcription. We used immunofluorescence to visualize the localization of the H1.5 to the centromere in astrocytes and performed chromatin immunoprecipitation which revealed an interaction of H1.5 with centromeric-protein A (CENP-A) nucleosomes in vivo in human cells. In vitro reconstitution of chromatin demonstrates that H1.5 can robustly bind to both CENP-A mono-nucleosomes and arrays of nucleosomes. Functionally, depletion of H1.5 from cells results in the loss of centromeric satellite transcription and leads to accumulation of mitotic defects. These data point to a hitherto unreported role for H1.5 in regulation of mitotic integrity in human cells.
Published in
Linker histone H1.5 contributes to centromere integrity
Saha A, Bui M, Melters DP et al. · Nucleic acids research 2026 · PMID 41521667 · doi:10.1093/nar/gkaf1400
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Also filed as BioProject PRJNA1011337 and SRA study SRP457835. Searching any of these in the dataset finder brings you back here.

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