Gcn5 and Spt3 can have opposite roles in regulating binding by the
TATA Binding Protein TBP.
Yaxin Yu, Peter Eriksson, David Stillman
Department of Pathology, University of Utah, 50 N. Medical Dr, Salt Lake
City, UT 84132-2501, USA
Transcriptional activation by RNA polymerase II requires binding of the
TATA-Binding Protein (TBP) to a promoter. Transcriptional activation of
the yeast HO gene requires many factors acting in sequence,
including the Gcn5 histone acetyltransferase, a component of the SAGA
complex. We show that expression of the yeast HO gene is
inhibited by the Spt3 protein, also a component of SAGA. Chromatin
immunoprecipitation experiments show that TBP binding to the HO
promoter is very weak in wild type cells, but markedly increased in an
spt3 mutant. In contrast, Spt3 stimulates TBP binding to the
GAL1 promoter (Dudley et al, Genes Dev 13:2940), and thus Spt3
regulates these two promoters differently . HO is not expressed
in a gcn5 mutant, but we show that HO is expressed in a
gcn5 spt3 double mutant. An spt20 mutation affects the
integrity of SAGA, and the fact that HO is expressed in an
spt20 mutant suggests that the major role of Gcn5 in HO
activation is to overcome repression by Spt3. Experiments with
SPT3 and SPT15 (encoding TBP) mutations that show allele
specific interaction demonstrate that interactions between Spt3 and TBP
are required to repress HO. We propose that Gcn5 and Spt3, both
in SAGA, have antagonizing effects on TBP binding to the HO
promoter, and act to severely limit HO expression within the cell
cycle.
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