Non-coding transcription SETs up regulation

• 来源期刊: 细胞研究（英文版）
• 年，卷（期）: 2013,（3）
• 页码范围: 311-313
• 页数: 3页
• 语种: 英文
• DOI: 10.1038/cr.2012.147

摘要

Transcription over a chromatin template is modulated by a number of post-translational modifications.Histone acetylation is a key activating mark that facilitates access to the DNA not only by impairing the ability of nucleosomes to bind the DNA tightly,but also by recruiting factors that aid the movement of the nucleosomes in cis or in trans.Therefore,in order to achieve a tight control over gene expression,it is imperative that the acetylation marks must be removed by histone lysine deacetylases (KDACs).While promoter acetylation is removed by the targeted recruitment of KDACs by repressor proteins,acetylation over the gene body is removed in a co-transcriptional manner.Studies from several labs have identified two RNA polymerase Ⅱ (RNAPII)-associated KDAC complexes [1] that act on the 5' (SET3 complex)and 3' (Rpd3S complex) ends of gene bodies (Figure 1A),maintaining nucleosomes in a hypoacetylated state [2,3].