Abstract
The general transcription factor TFIID and its individual subunits (TAF(II)s) have been the focus of many studies, yet their functions in vivo are not well established. Here we characterize the requirement of yeast TAF(II)s for the derepression of the ribonucleotide reductase (RNR) genes. Promoter mapping studies revealed that the upstream repressing sequences, the damage-responsive elements (DREs), rendered these genes dependent upon TAF(II)s. DREs are the binding sites for the sequence-specific DNA binding-protein Crt1 that represses transcription by recruiting the Ssn6-Tup1 co-repressor complex to the promoter. We demonstrate that deletion of SSN6, TUP1 or CRT1 alleviated the TAF(II) dependence of the RNR genes, indicating that TAF(II) dependence requires the co-repressor complex. Furthermore, we provide evidence that Crt1 specifies the TAF(II) dependence of these genes. Our studies show that TFIID interacts with the repression domain of Crt1, suggesting that the derepression mechanism involves an antagonism between TFIID and the co-repressor complex. Our results indicate that yeast TAF(II)s have other functions in addition to core promoter selectivity, and describe a novel activity: the derepression of promoters.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
