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J. Biol. Chem., Vol. 276, Issue 18, 14685-14694, May 4, 2001
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From the Institute of Molecular Medicine and Genetics and
Department of Radiology, Medical College of Georgia,
Augusta, Georgia 30912
The heat shock transcription factors (HSFs)
regulate the expression of heat shock proteins (hsps), which are
critical for normal cellular proliferation and differentiation. One of
the HSFs, HSF-4, contains two alternative splice variants, one of which
possesses transcriptional repressor properties in vivo. This repressor isoform inhibits basal transcription of hsps 27 and 90 in tissue culture cells. The molecular mechanisms of HSF-4a isoform-mediated transcriptional repression is unknown. Here, we
present evidence that HSF-4a inhibits basal transcription in vivo when it is artificially targeted to basal promoters via the DNA-binding domain of the yeast transcription factor, GAL4. By using a
highly purified, reconstituted in vitro transcription system, we show that HSF-4a represses basal transcription at an early
step during preinitiation complex assembly, as pre-assembled preinitiation complexes are refractory to the inhibitory effect on
transcription. This repression occurs by the HSF-4a isoform, but not by
the HSF-4b isoform, which we show is capable of activating transcription from a heat shock element-driven promoter in
vitro. The repression of basal transcription by HSF-4a occurs
through interaction with the basal transcription factor TFIIF. TFIIF
interacts with a segment of HSF-4a that is required for the
trimerization of HSF-4a, and deletion of this segment no longer
inhibits basal transcription. These studies suggest that HSF-4a
inhibits basal transcription both in vivo and in
vitro. Furthermore, this is the first report identifying an
interaction between a transcriptional repressor with the basal
transcription factor TFIIF.
Heat Shock Factor-4 (HSF-4a) Represses Basal Transcription
through Interaction with TFIIF*
*
This work was supported by NCI Grants CA85947 and CA62130
from the National Institutes of Health.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Institute of Molecular
Medicine and Genetics and Dept. of Radiology, Medical College of
Georgia, 1120, 15th St., CB2803, Augusta, GA 30912. Tel.: 706-721-8759; Fax: 706-721-8752; E-mail: mivechi@immag.mcg.edu.
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