Co-localization of elements required for phorbol ester stimulation and glucocorticoid repression of proliferin gene expression.

J. C. Mordacq*, D. I. Linzer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

124 Scopus citations

Abstract

Proliferin (PLF) gene expression provides a model of growth-related transcriptional activation in mouse cells. Transcription from a cloned PLF promoter is inducible by phorbol esters, and this induction involves a region of 31 bp that includes an AP-1 site and a cluster of sites similar to the simian virus 40 (SV40) SphI element. The mutation of either the AP-1 or the SphI sites abolishes phorbol ester induction, and the transfer of this 31-bp sequence to a site upstream of a minimal promoter is sufficient to confer phorbol-ester responsiveness. In contrast to phorbol esters, glucocorticoids repress PLF transcription, which results in a reduced accumulation of PLF mRNA in serum-stimulated cells. Repression is dependent on the glucocorticoid receptor, which binds to the PLF promoter in a region that includes the AP-1 site, and the 31-bp phorbol ester 12-O-tetra decanoylphorbol-13-acetate (TPA)-inducible region is sufficient to mediate glucocorticoid repression. In addition, extracts from glucocorticoid-treated and untreated mouse cells are found to differ in the nature of the protein complexes that interact with the AP-1 site.

Original languageEnglish (US)
Pages (from-to)760-769
Number of pages10
JournalGenes & development
Volume3
Issue number6
DOIs
StatePublished - Jun 1989

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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