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


Name: Prelich, Greg
Mailing Address: Molecular Genetics, Albert Einstein College of Med, 1300 Morris Park Ave, Bronx, NY 10461, USA
Email Address: prelich@aecom.yu.edu
Phone and Fax numbers: (718)-430-2181, (718)-430-8778

019

Hyperactive TATA-binding protein mutants.


Yong Cang, Greg Prelich
Molecular Genetics, Albert Einstein College of Med, 1300 Morris Park Ave, Bronx, NY 10461, USA

In an effort to identify proteins that have general roles in transcription by RNA polymerase II, we have previously selected for mutations that cause increased transcription from suc2deltauas (a transcriptionally inactive allele of SUC2 ). Our original selection identified recessive mutations in six BUR genes ( BUR = Bypass UAS Requirement) that encode general repressors of transcription. Bur3 (=Mot1) and Bur6 repress transcription by directly inhibiting the TATA-binding protein (TBP), while the other Bur proteins have been proposed to inhibit transcription via chromatin-mediated repression. Here we describe a new class of bur mutations. We have mutagenized the gene that encodes yeast TBP ( SPT15 ), selecting for TBP mutations that increase transcription from suc2deltauas . TBP alleles arising from this selection were expected to be UAS-independent either due to loss of repression or due to an increase of an intrinsic TBP activity. The majority of our TBP mutations (34 out of 36) map to a very tight cluster of residues on the exposed surface of TBP. This cluster is likely to define a previously unidentified interface for contact with a repressor of TBP. In addition to these clustered mutations, we have also identified two other Bur - TBP surface mutations: the first shows genetic interactions with MOT1 , while the second mutation lies on the DNA-binding surface of TBP. We will present further genetic and biochemical analysis of these hyperactive TBP alleles.


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