E1A-dependent trans-activation of the c-fos promoter requires the TATAA sequence

M. C. Simon, Robert Rooney, T. M. Fisch, N. Heintz, J. R. Nevins

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Previous experiments have demonstrated that transcription of the human c-fos oncogene is activated through the action of the 289-amino acid adenovirus E1A gene product. In this study we have utilized a series of c-fos promoter deletion and substitution mutants to define regulatory sequences that allow the induction by E1A. Although the deletion of upstream promoter sequences has varying degrees of effect on overall promoter activity, these deletions retain inducibility by E1A. This includes the deletion of the serum response element and two elements that bind the ATF transcription factor. In fact, a c-fos promoter deleted to position -53, which leaves the TATA element but no other known functional elements, retains inducibility, indicating a role for the TATA element in E1A control. Indeed, substitution of the c-fos TAA element (TATAA) with a TATA sequence from the simian virus 40 early promoter (TATTTAT) abolishes E1A inducibility; this promoter does retain responsiveness to cAMP induction, however, demonstrating that this TATTTAT substitution is functional. We conclude that the E1A-dependent activation of c-fos transcription is mediated through an effect on a TATA-binding protein that has specificity for the TATAA sequence.

Original languageEnglish (US)
Pages (from-to)513-517
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number2
DOIs
StatePublished - Jan 1 1990

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Serum Response Element
Activating Transcription Factors
TATA-Box Binding Protein
Simian virus 40
Oncogenes
Adenoviridae
Amino Acids
Genes

All Science Journal Classification (ASJC) codes

  • General

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E1A-dependent trans-activation of the c-fos promoter requires the TATAA sequence. / Simon, M. C.; Rooney, Robert; Fisch, T. M.; Heintz, N.; Nevins, J. R.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 87, No. 2, 01.01.1990, p. 513-517.

Research output: Contribution to journalArticle

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