Yeast Genetics and Molecular Biology 2002
University of Wisconsin
Madison, Wisconsin USA
July 30 - August 4, 2002


Name: Jaehning, Judith A.
Mailing Address: Molecular Biology Program, University of Colorado HSC, 4200 E. 9th Ave., Denver, CO 80262, USA
Email Address: Judith.Jaehning@UCHSC.edu
Phone & FAX numbers: 303 315 3004 & 303 315 3326

Abstract #47


Session Title: Transcription, Elongation and Termination
Session Time: Friday, August 2 -- 11:00AM - 12:30PM
Presentation: Platform
Topic: Gene Expression

Biochemical and genetic characterization of the Paf1/RNA polymerase II complex.
Cherie L. Mueller (1), Judith A. Jaehning (2)
(1) Department of Biochemistry and Molecular Genetics; (2) Molecular Biology Program, University of Colorado HSC, 4200 E. 9th Ave., Denver, CO 80262, USA

The yeast Paf1/RNA polymerase II (pol II) complex is biochemically and functionally distinct from the Srb-mediator form of pol II holoenzyme, and is required for full expression of a subset of genes including many of those whose expression is regulated during the cell cycle, including CLN1, HO and RNR1. Using Tandem Affinity Purification (TAP) tags and mass-spectrometry we isolated the Paf1 complex and identified additional components including Ctr9, Rtf1 and Leo1. paf1 and ctr9 strains have very similar pleiotropic phenotypes, which are unaltered when the two mutations are combined. In contrast, deletion of LEO1 or RTF1 leads to few obvious phenotypes, but combining leo1 or rtf1 with paf1 leads to suppression of many paf1 phenotypes including slow growth, and sensitivity to high temperature, caffeine and hydroxyurea. In addition, expression of several genes whose expression is reduced in paf1 is restored to wild type levels in the rtf1 paf1 double mutant. Using chromatin immuno-precipitation, we have found that Paf1 complex component Leo1 can be detected throughout the length of the CLN1 and HO genes in wild type cells. In a paf1 mutant the Leo1 signal is dramatically reduced in concert with the reduced expression of the genes. We are currently testing the hypothesis that lack of Paf1 results in a defective complex and a block in transcription, which is relieved by removal of Leo1 or Rtf1.


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