A chromatin-based mechanism for limiting divergent non-coding transcription. Saccharomyces cerevisiae BY4741

In addition to their annotated transcript, many eukaryotic mRNA promoters also produce unstable divergent non-coding transcripts. We show that sequences in the non-coding transcript, rather than the promoter, determine the termination and RNA decay pathway used. Functional protein-coding transcripts can be produced in the divergent direction. We identify chromatin assembly as key mechanism repressing divergent non-coding transcription by measuring promoter directionality in the collection of non-essential yeast deletion mutants using fluorescent reporter genes. The CAF-I complex represses nascent divergent non-coding transcription genome-wide. In contrast, H3K56 hyperacetylation and the nucleosome remodeler SWI/SNF promote rapid nucleosome turnover to increase divergent transcription. Chromatin-based amplification and repression is linked to asymmetric H3K56 acetylation at promoters to tune divergent transcription each direction. We propose that chromatin-mediated effects control divergent transcription, complementing downstream pathways linked to early termination and degradation of the non-coding RNAs.