Repression of Divergent Noncoding Transcription by a Sequence-Specific Transcription Factor

作     者：Wu, Andrew C. K. Patel, Harshil Chia, Minghao Moretto, Fabien Frith, David Snijders, Ambrosius P. van Werven, Folkert J. 

作者机构：Francis Crick Inst Cell Fate & Gene Regulat Lab 1 Midland Rd London NW1 1AT England Francis Crick Inst Bioinformat & Biostat 1 Midland Rd London NW1 1AT England Francis Crick Inst Prot Anal & Prote Platform 1 Midland Rd London NW1 1AT England 

出 版 物：《MOLECULAR CELL》 (分子细胞)

年 卷 期：2018年第72卷第6期

页      面：942-+页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 07[理学] 

基　　金：Francis Crick Institute [FC001203] Cancer Research UK [FC001203] UK Medical Research Council [FC001203] Wellcome Trust [FC001203] Agency for Science, Technology and Research (A*STAR) of Singapore 

主　　题：yeast RSC promoter Rap1 transcription divergent noncoding RNA transcription factor repression directionality 

摘      要：Many active eukaryotic gene promoters exhibit divergent noncoding transcription, but the mechanisms restricting expression of these transcripts are not well understood. Here, we demonstrate how a sequence-specific transcription factor represses divergent noncoding transcription at highly expressed genes in yeast. We find that depletion of the transcription factor Rap1 induces noncoding transcription in a large fraction of Rap1-regulated gene promoters. Specifically, Rap1 prevents transcription initiation at cryptic promoters near its binding sites, which is uncoupled from transcription regulation in the protein-coding direction. We further provide evidence that Rap1 acts independently of previously described chromatin-based mechanisms to repress cryptic or divergent transcription. Finally, we show that divergent transcription in the absence of Rap1 is elicited by the RSC chromatin remodeler. We propose that a sequence-specific transcription factor limits access of basal transcription machinery to regulatory elements and adjacent sequences that act as divergent cryptic promoters, thereby providing directionality toward productive transcription.