The protooncogene c-jun contains an unusual estrogen-inducible enhancer within the coding sequence

S. M. Hyder, Zafar Nawaz, C. Chiappetta, K. Yokoyama, G. M. Stancel

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Estrogens have previously been shown to induce c-jun mRNA levels in target cells during hormone induced proliferation, and this appears to be a primary hormonal response involving transcriptional activation. In this report we have now identified an estrogen dependent enhancer within the coding sequence of c-jun. This element has the sequence GCAGAnnnTGACC which is identical to the consensus estrogen response element GGTCAnnnTGACC in the second half site, but varies considerably in the first half site. Synthetic oligodeoxynucleotides containing this jun sequence bind the estrogen receptor in cell-free studies using a competitive band shift assay with the consensus element. The jun element also confers hormone inducibility to reporter plasmids in yeast and mammalian based transcriptional systems. Structure-function studies illustrate that the TGACC half-site and its immediate flanking dinucleotides, but not the GCAGA half-site, are required for estrogen receptor binding. In contrast, both the GCAGA and TGACC half- sites are obligatory for hormone-inducible transcriptional activation. These results suggest a model in which the estrogen receptor functions as a heterodimer to regulate transcription of the c-jun protooncogene. Coupled with reports of estrogen response elements in c-fos and estrogenic induction of c-fos and c-jun in vivo, these findings also support a role for AP-1 components as early response genes in estrogen-induced proliferation.

Original languageEnglish
Pages (from-to)8506-8513
Number of pages8
JournalJournal of Biological Chemistry
Volume270
Issue number15
DOIs
StatePublished - Jan 1 1995
Externally publishedYes

Fingerprint

Estrogens
Estrogen Receptors
Response Elements
Hormones
Transcriptional Activation
Chemical activation
Oligodeoxyribonucleotides
Transcription Factor AP-1
Transcription
Yeast
Assays
Plasmids
Genes
Yeasts
Messenger RNA

ASJC Scopus subject areas

  • Biochemistry

Cite this

The protooncogene c-jun contains an unusual estrogen-inducible enhancer within the coding sequence. / Hyder, S. M.; Nawaz, Zafar; Chiappetta, C.; Yokoyama, K.; Stancel, G. M.

In: Journal of Biological Chemistry, Vol. 270, No. 15, 01.01.1995, p. 8506-8513.

Research output: Contribution to journalArticle

Hyder, S. M. ; Nawaz, Zafar ; Chiappetta, C. ; Yokoyama, K. ; Stancel, G. M. / The protooncogene c-jun contains an unusual estrogen-inducible enhancer within the coding sequence. In: Journal of Biological Chemistry. 1995 ; Vol. 270, No. 15. pp. 8506-8513.
@article{131e0e13792e4b6ca2619c63fa851372,
title = "The protooncogene c-jun contains an unusual estrogen-inducible enhancer within the coding sequence",
abstract = "Estrogens have previously been shown to induce c-jun mRNA levels in target cells during hormone induced proliferation, and this appears to be a primary hormonal response involving transcriptional activation. In this report we have now identified an estrogen dependent enhancer within the coding sequence of c-jun. This element has the sequence GCAGAnnnTGACC which is identical to the consensus estrogen response element GGTCAnnnTGACC in the second half site, but varies considerably in the first half site. Synthetic oligodeoxynucleotides containing this jun sequence bind the estrogen receptor in cell-free studies using a competitive band shift assay with the consensus element. The jun element also confers hormone inducibility to reporter plasmids in yeast and mammalian based transcriptional systems. Structure-function studies illustrate that the TGACC half-site and its immediate flanking dinucleotides, but not the GCAGA half-site, are required for estrogen receptor binding. In contrast, both the GCAGA and TGACC half- sites are obligatory for hormone-inducible transcriptional activation. These results suggest a model in which the estrogen receptor functions as a heterodimer to regulate transcription of the c-jun protooncogene. Coupled with reports of estrogen response elements in c-fos and estrogenic induction of c-fos and c-jun in vivo, these findings also support a role for AP-1 components as early response genes in estrogen-induced proliferation.",
author = "Hyder, {S. M.} and Zafar Nawaz and C. Chiappetta and K. Yokoyama and Stancel, {G. M.}",
year = "1995",
month = "1",
day = "1",
doi = "10.1074/jbc.270.15.8506",
language = "English",
volume = "270",
pages = "8506--8513",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "15",

}

TY - JOUR

T1 - The protooncogene c-jun contains an unusual estrogen-inducible enhancer within the coding sequence

AU - Hyder, S. M.

AU - Nawaz, Zafar

AU - Chiappetta, C.

AU - Yokoyama, K.

AU - Stancel, G. M.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Estrogens have previously been shown to induce c-jun mRNA levels in target cells during hormone induced proliferation, and this appears to be a primary hormonal response involving transcriptional activation. In this report we have now identified an estrogen dependent enhancer within the coding sequence of c-jun. This element has the sequence GCAGAnnnTGACC which is identical to the consensus estrogen response element GGTCAnnnTGACC in the second half site, but varies considerably in the first half site. Synthetic oligodeoxynucleotides containing this jun sequence bind the estrogen receptor in cell-free studies using a competitive band shift assay with the consensus element. The jun element also confers hormone inducibility to reporter plasmids in yeast and mammalian based transcriptional systems. Structure-function studies illustrate that the TGACC half-site and its immediate flanking dinucleotides, but not the GCAGA half-site, are required for estrogen receptor binding. In contrast, both the GCAGA and TGACC half- sites are obligatory for hormone-inducible transcriptional activation. These results suggest a model in which the estrogen receptor functions as a heterodimer to regulate transcription of the c-jun protooncogene. Coupled with reports of estrogen response elements in c-fos and estrogenic induction of c-fos and c-jun in vivo, these findings also support a role for AP-1 components as early response genes in estrogen-induced proliferation.

AB - Estrogens have previously been shown to induce c-jun mRNA levels in target cells during hormone induced proliferation, and this appears to be a primary hormonal response involving transcriptional activation. In this report we have now identified an estrogen dependent enhancer within the coding sequence of c-jun. This element has the sequence GCAGAnnnTGACC which is identical to the consensus estrogen response element GGTCAnnnTGACC in the second half site, but varies considerably in the first half site. Synthetic oligodeoxynucleotides containing this jun sequence bind the estrogen receptor in cell-free studies using a competitive band shift assay with the consensus element. The jun element also confers hormone inducibility to reporter plasmids in yeast and mammalian based transcriptional systems. Structure-function studies illustrate that the TGACC half-site and its immediate flanking dinucleotides, but not the GCAGA half-site, are required for estrogen receptor binding. In contrast, both the GCAGA and TGACC half- sites are obligatory for hormone-inducible transcriptional activation. These results suggest a model in which the estrogen receptor functions as a heterodimer to regulate transcription of the c-jun protooncogene. Coupled with reports of estrogen response elements in c-fos and estrogenic induction of c-fos and c-jun in vivo, these findings also support a role for AP-1 components as early response genes in estrogen-induced proliferation.

UR - http://www.scopus.com/inward/record.url?scp=0028969414&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028969414&partnerID=8YFLogxK

U2 - 10.1074/jbc.270.15.8506

DO - 10.1074/jbc.270.15.8506

M3 - Article

VL - 270

SP - 8506

EP - 8513

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 15

ER -