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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 GCAGA nnnTGACC
which is identical to the consensus estrogen response element
GGTCA nnnTGACC 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.
Volume 270,
Number 15,
Issue of April 14, pp. 8506-8513, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
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