The CUP1 upstream repeated element renders CUP1 promoter activation insensitive to mutations in the RNA polymerase II transcription complex
Author(s) -
Laura Badi
Publication year - 2002
Publication title -
nucleic acids research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 9.008
H-Index - 537
eISSN - 1362-4954
pISSN - 0305-1048
DOI - 10.1093/nar/30.6.1306
Subject(s) - biology , rna polymerase ii , transcription (linguistics) , gene , genetics , locus (genetics) , rna polymerase , promoter , transcription factor , rna , gene expression , linguistics , philosophy
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.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom