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Background：
Canonical histone H2B heterodimerizes with H2A to assemble the core nucleosome particle. Reversible lysine acetylation on the flexible N-terminal tail of H2B is a classic marker of transcription-permissive chromatin. Acetylation neutralizes positive charges of histone tails, weakens histone-DNA interaction and creates binding sites for bromodomain-containing co-activators. Different lysine sites on H2B tail carry distinct functions in transcription initiation, elongation and post-damage chromatin recovery. 2B Lys5 acetylation (H2B K5ac) is catalyzed by p300/CBP and accumulates at active gene promoters and enhancers. Multi-site acetylation of H2B N-tail synergistically relaxes chromatin and recruits transcriptional co-activators. H2B K5ac co-localizes with active enhancer marker H3K27ac and dynamically changes during cell cycle progression and cell differentiation. H2B Lys11 acetylation (H2B K11ac) is modified by GCN5 and p300/CBP, distributed across gene promoters and coding regions to facilitate RNA polymerase II elongation. Oxidative stress or DNA damage induces rapid deacetylation of H2B K11, repressing survival and repair genes and triggering cell cycle arrest. The acetylation level of this site positively correlates with overall gene expression intensity.
