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Acetylation of histone tails plays a key role in chromatin dynamics and is associated with the potential for gene expression. We show here that a 2-3 bp mispositioning of the nucleosome covering the TATA box at PHO5 induces a dependency on the acetylatable lysine residues of the histone H4 N-terminal region and on the TFIID-associated bromodomain factor Bdf1. This dependency arises either through fusion of the PHO5 promoter to a lacZ reporter or by mutation of the TATA box in the natural gene. The results suggest that promoters in which the TATA box is either absent or poorly accessible on the surface of a nucleosome may compensate by using Bdf1 bromodomains and acetylated H4 tails to anchor TFIID to the promoter during the initial stages of transcription activation. We propose that nucleosome positioning at the nucleotide level provides a subtle, but highly effective, mechanism for gene regulation.

Original publication




Journal article


Mol Cell

Publication Date





69 - 81


Acetylation, Acid Phosphatase, Base Pair Mismatch, Carrier Proteins, Cells, Cultured, Gene Expression Regulation, Fungal, Histones, Lac Operon, Lysine, Mutation, Nucleosomes, RNA, Messenger, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, TATA Box, Transcription Factor TFIID, Transcription Factors, Transcriptional Activation