Identification of silencer binding proteins from yeast: possible roles in SIR control and DNA replication

• Published in: The EMBO journal Vol. 6; no. 2; pp. 461 - 467
• Main Authors: Shore, David, Stillman, David J., Brand, Andrea H., Nasmyth, Kim A.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group 01.02.1987
• Subjects: ARS elements; Biological and medical sciences; DNA binding proteins; DNA Replication - genetics; Fundamental and applied biological sciences. Psychology; Genes, Fungal - genetics; Genes, Mating Type, Fungal; mating type; Molecular and cellular biology; Molecular genetics; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae Proteins - genetics; silencer; Silencer Elements, Transcriptional - genetics; Silent Information Regulator Proteins, Saccharomyces cerevisiae - genetics; Transcription. Transcription factor. Splicing. Rna processing; transcriptional control; Binding protein; Regulation(control); Yeast; Transcription; DNA; Inheritance; Replication; Gene expression; Mating type
• ISSN: 0261-4189; 1460-2075
• DOI: 10.1002/j.1460-2075.1987.tb04776.x

The ‘silent’ yeast mating‐type loci (HML and HMR) are repressed by sequences (HMLE and HMRE) located over 1 kb from their promoters which have properties opposite those of enhancers, and are called ‘silencers’. Both silencers contain autonomously replicating sequences (ARS). Silencer activity requires four trans‐acting genes called SIR (silent information regulator). We have identified two DNA binding factors, SBF‐B and SBF‐E, which bind to known regulatory elements at HMRE. SBF‐B binds to a region involved in both the silencer and ARS functions of HMRE, but does not bind to HMLE. This factor also binds to the unlinked ARS1 element. SBF‐E recognizes a sequence found at both silencers. These results suggest that the two silencers may be composed of different combinations of regulatory elements at least one of which is common to both. Neither factor appears to be a SIR gene product. Hence the SIR proteins may not directly interact with the silencer control sites.