ArticleNature communications2026
Site-specific programming characterizes dynamic post-translational acetylation of histone H2B lysine 108 in mouse embryonic stem cells.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Dynamic histone modifications are critical for regulating stem cell fate. However, generalized strategies for site-specific programming of histone modifications profiling on unperturbed chromatin in embryonic stem cells (ESCs) remain challenging. In this study, we established a genetic code expansion-based platform in mouse ESCs (mESCs) for site-specific proteomic mapping and functional analysis within native chromatin. Using this platform, we revealed Rps19bp1 promotes Sirt1-mediated deacetylation of histone H2B lysine 108 acetylation (H2B-K108ac). Moreover, Site-specific-AcK revealed that H2B-K108ac induces the formation of H2B puncta and modulates chromatin accessibility. Functionally, elevation of H2B-K108ac via genetic code expansion and the loss of Rps19bp1 cause significant alterations in the expression of genes associated with mESC differentiation. Furthermore, Rps19bp1 deficiency promotes neural differentiation in mESC-derived teratoma. Our study develops a robust platform for linking specific histone acetylation with chromatin dynamics and cell fate determination, which lays a foundation for future exploration of additional histone PTMs in ESCs.
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