Martinez-Campa Carlos, Politis Panagiotis, Moreau Jean-Luc, Kent Nick, Goodall Jane, Mellor Jane, Goding Colin R
Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, United Kingdom.
Mol Cell. 2004 Jul 2;15(1):69-81. doi: 10.1016/j.molcel.2004.05.022.
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.
组蛋白尾巴的乙酰化在染色质动态变化中起关键作用，并与基因表达潜力相关。我们在此表明，覆盖PHO5基因TATA盒的核小体发生2 - 3个碱基对的错位，会导致对组蛋白H4 N端区域可乙酰化赖氨酸残基以及与TFIID相关的溴结构域因子Bdf1产生依赖。这种依赖可通过将PHO5启动子与lacZ报告基因融合，或通过天然基因中TATA盒的突变而产生。结果表明，在核小体表面TATA盒缺失或难以接近的启动子，可能在转录激活初始阶段通过利用Bdf1溴结构域和乙酰化H4尾巴将TFIID锚定到启动子上来进行补偿。我们提出，核苷酸水平的核小体定位为基因调控提供了一种微妙但高效的机制。
