To determine the genome-wide localization and redistribution of histone H3 lysine 18 acetylation (H3K18ac) induced by the adenovirus small e1a oncoprotein in normal host cells.
Expressed the adenovirus small e1a oncoprotein in normal, contact-inhibited fibroblasts.
Performed chromatin immunoprecipitation sequencing (ChIP-seq) 24 hours post-expression to map genome-wide changes in H3K18ac and H3K9ac marks alongside RB-family protein binding loci.
E1a eliminated 95% of preexisting H3K18ac peaks—specifically at promoters and intergenic regions of fibroblast-related genes—and established one-third as many new peaks at promoters of cell-cycle genes and putative enhancers.
New H3K18ac peaks formed at sites bound by retinoblastoma-family proteins in quiescent cells, including 55% of RB1-bound genomic loci.
More than 50% of H3K9ac peaks retained their genomic distribution before and after viral infection independently of RB1.
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