Figure 2.

Possible mechanisms for the regulation of genome expression by non-coding transcription. (A) Bidirectional PARs and mRNAs might originate from different pre-initiation complexes (PICs) and compete for the same pool of transcription factors to initiate transcription. Binding of TBP or other factors might be responsible for directing the balance towards mRNA synthesis. (B) The transcriptional interference mechanism, in which transcription factors (TFs) are displaced from the mRNA promoter by the upstream cryptic transcription, is shown. The SRG1 cryptic non-coding RNA (ncRNA) interferes with the promoter of the downstream SER3 gene through this mechanism. (C) Model for start site selection. The CUT and the mRNA have the same promoter but originate from different transcription start sites and compete for the same pool of PIC factors. An example of this type of regulation occurs at the IMD2 locus. (D) Transcription-induced chromatin modifications, in which cryptic transcription modifies promoter proximal chromatin to attenuate gene expression. The GAL10–GAL1 locus is regulated through this mechanism; cryptic transcription that originates upstream from the GAL10–GAL1 promoter induces the methylation of H3K4 and/or H3K36 by the HMTs Set1 and Set2, respectively, and tethers the Rpd3S histone deacetylase complex to attenuate gene expression of the GAL locus. CUT, cryptic unstable transcript; H3, histone H3; HMT, histone methyl transferase; IMD2, inosine monophosphate dehydrogenase 2; K, lysine; PAR, promoter-associated non-coding RNA; Rpd3S, reduced potassium dependency 3 small; SER3, serine requiring 3; Set1/2, SET-domain-comtaining 1/2; SRG1, SER3 regulatory gene; TBP, TATA binding protein.