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


Name: Mathias, Jonathan
Mailing Address: Waksman Institute, Rutgers University, 190 Frelinghuysen Rd, Piscataway, NJ 08854, USA
Email Address: jmathias@eden.rutgers.edu
Phone & FAX numbers: (732) 445-3901 & (732) 445-5735

Abstract #359


Session Title: Gene Expression: Transcriptional Regulation
Presentation: Poster
Topic: Gene Expression

Repression of the HO gene by the alpha2 and a1 homeodomain proteins.
Jonathan Mathias, Andrew Vershon
Waksman Institute, Rutgers University, 190 Frelinghuysen Rd, Piscataway, NJ 08854, USA

The homeodomain is a highly conserved DNA-binding motif found in transcriptional regulators from yeast to humans. The yeast MATalpha2 and MATa1 homeodomain proteins form a heterodimer (alpha2/a1) that binds DNA upstream of several haploid-specific genes to repress their transcription in the diploid cell type. One such gene is HO, which encodes a protein that initiates mating type switching in haploid yeast. Expression of HO is regulated by an extensive promoter that resembles promoters found in higher-ordered eukaryotes, and alpha2/a1 represses HO transcription by binding to ten sites within this promoter. We show that alpha2/a1 binds to these individual sites with differing affinity, and potentially regulates HO through cooperative interactions between alpha2/a1 heterodimers bound to strong and weak-affinity sites. The alpha2/a1 complex represses target genes through interactions with the Tup1/Ssn6 corepressor, which interacts with subunits of the Srb/Mediator complex as well as several histone deacetylases. We will report on the progress of determining the factors that repress HO in diploid yeast in conjunction with alpha2/a1 and Tup1/Ssn6, and whether these repressor proteins prevent DNA-binding and transcription regulation by Swi5/Pho2 and other HO activators. These and other experiments will determine whether alpha2/a1 acts in a local manner around each individual binding site, or if a repressive chromatin environment is set up across the promoter.


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