Yeast Genetics and Molecular Biology 1998
College Park, Maryland
August 1998


Name: Stargell, Laurie A.
Mailing Address: Biochemistry & Molecular Biol., Colorado State University, MRB, Fort Collins, CO 80523-1870, USA
Email Address: lstargell@vines.colostate.edu
Phone and Fax numbers: 970-491-5068, 970-491-0494

018

Characterization of a TBP mutant defective for TATA-less transcription in vivo.


Ryan T. Ranallo (1), Kevin Struhl (2), Laurie A. Stargell (1)
(1) Biochemistry & Molecular Biol., Colorado State University, MRB, Fort Collins, CO 80523-1870, USA; (2) Harvard Medical School, 240 Longwood Ave, Boston, MA 02215

In RNA polymerase II transcription, TBP functions in a multi-subunit complex (TFIID) that consists of TBP and TBP associated factors (TAFs). TBP is also required for transcription by Pol I and Pol III. Here, we present the initial characterization of a yeast temperature-sensitive TBP mutant (K151L; K156Y) that is specifically defective for Pol II transcription. This TBP mutant is functional for both Pol I and Pol III transcription, and also appears to be functional for basal and activated transcription from Pol II promoters containing a TATA element. In contrast, this allele may be defective for transcriptional activity at promoters lacking a canonical TATA element. Currently it is not known whether there is a difference between the mechanism of transcription at TATA-containing and TATA-less promoters. To determine the specificity of this defect we are expanding our studies to include newly designed probes for other TATA-less promoters. Initial biochemical data indicates that this TBP mutant does not remain part of an intact TFIID complex at the non-permissive temperature (the mutant TFIID is severely depleted for various TAFs). An attractive hypothesis that is also supported by work from other laboratories is that certain TAFs are more critical at TATA-less promoters. Using site-directed mutagenesis we have created single mutants at amino acid 151 or 156 and found that both mutations are required for the lethal phenotype at the non-permissive temperature. Future studies may allow us to more clearly define the role of TBP in transcription by Pol II at TATA-less promoters.


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