The CUP1 upstream repeated element renders CUP1 promoter activation insensitive to mutations in the RNA polymerase II transcription complex.
Activation of transcription in eukaryotes requires the concerted action of numerous components of the RNA polymerase II transcriptional apparatus. The degree of dependence on many of these components varies from gene to gene and it is still largely unknown how the requirement for any particular component is determined at any given gene. We show that removal of Gal11 from the yeast transcription complex can affect activation from the CUP1 UAS in a manner dependent on its genomic context. Our results indicate a novel function for the CUP1 upstream repeated element (CURE) located upstream of the CUP1 UAS at the naturally multimerized CUP1 locus. The presence of CURE endowed the CUP1 UAS with a reduced susceptibility to the effects of deleting Gal11. Similar results were obtained with the Srb/mediator subunit Srb5. Restoration of activation from the CUP1 promoter to wild-type levels by the CURE correlated with changes in the accessibility of local chromatin to nucleases. The CURE sequence may serve to protect the stress-inducible CUP1 UAS-promoter elements against reduced activation that may result from crippled transcription complexes under stress conditions.[1]References
- The CUP1 upstream repeated element renders CUP1 promoter activation insensitive to mutations in the RNA polymerase II transcription complex. Badi, L., Barberis, A. Nucleic Acids Res. (2002) [Pubmed]
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