Transcriptional activation by SP1 as directed through TATA or initiator: Specific requirement for mammalian transcription factor IID
Abstract
Transcription of mammalian genes by RNA polymerase II often begins at a specific nucleotide, whose location is determined either by an upstream DNA element known as a TATA box or by an element positioned at the transcription start site called an initiator (Inr). By in vitro analysis of synthetic promoters, we demonstrate here that the TATA and Inr elements are functionally similar and that the Inr is contained between nucleotides -3 and +5 relative to the initiation site. Moreover, we found that a mammalian transcription factor IID (TFIID) protein fraction is required for transcriptional stimulation by an Sp1-dependent activating element placed upstream of either TATA or Inr elements. However, in these assays, the yeast TATA-binding protein, which previously was shown to function similarly to mammalian TFIID, could not efficiently substitute for the mammalian TFIID fraction. These results demonstrate that mammalian TFIID is functionally distinct from the yeast TATA-binding protein and may contain additional subunits or domains that are important for transcriptional activation from some promoters.
Additional Information
© 1990 by the National Academy of Sciences. Contributed by David Baltimore, March 26, 1990. We are grateful to Frank Pugh and Robert Tjian for discussing results prior to their publication, to Qiang Zhou for important contributions, and to Donald Rio for the use of his FPLC apparatus. We also thank Doug Black, Paul Kaufman, Donald Rio, and Marilyn Smith for critical reading of the manuscript. This work was supported by postdoctoral fellowships from the Helen Hay Whitney Foundation (S.T.S.), Arthritis Foundation (S.T.S.), and American Cancer Society (M.C.S.; PF2715), and by grants from the National Cancer Institute (A.J.B.; CA41062 and CA25235), American Cancer Society (D.B.; IM355T), Public Health Service (D.B.; GM39458), and the DuPont Center for Molecular Genetics (D.B.). The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.Attached Files
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Additional details
- PMCID
- PMC54145
- Eprint ID
- 9219
- Resolver ID
- CaltechAUTHORS:SMApnas90
- Helen Hay Whitney Foundation
- Arthritis Foundation
- American Cancer Society
- PF2715
- NIH
- CA41062
- NIH
- CA25235
- American Cancer Society
- IM355T
- NIH
- GM39458
- DuPont Center for Molecular Genetics
- Created
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2007-11-27Created from EPrint's datestamp field
- Updated
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2021-11-08Created from EPrint's last_modified field