Figure 8. The GAL cluster lncRNAs poise the protein-coding GAL genes for rapid induction from repressive conditions.

Transcriptional repression of the protein-coding GAL genes occurs through binding of glucose-responsive transcriptional repressors (Rep) and subsequent recruitment of co-repressors Tup1–Cyc8 to gene promoters (repression) [28], [32], [46]–[48], [51]. Derepression is accomplished through lncRNA-dependent displacement of these repressors from chromatin. Displacement may occur through transcriptional interference and/or formation of RNA–DNA hybrids between the lncRNA and targeted, protein-coding gene. Derepression is transient, however, due to the action of Dbp2 and Xrn1, which facilitate lncRNA release from chromatin and RNA decay, respectively. This equilibrium between repressed and derepressed states allows for faster transcriptional activation in the presence of galactose. Activation then requires release of the Gal80 inhibitor protein from the Gal4 activator and subsequent recruitment of coactivating complexes and RNAPII (not pictured) [29]. Thus, the GAL lncRNAs function at the temporal level of gene regulation by enhancing the kinetics of GAL gene induction from transcriptionally repressive conditions.