AP-1/jun binding sites mediate serum inducibility of the human vimentin promoter

Nucleic Acids Res. 1989 Feb 25;17(4):1619-33. doi: 10.1093/nar/17.4.1619.

Abstract

The vimentin gene is inducible by serum in quiescent Balb/c 3T3 cells, but the molecular mechanism of this induction is unknown. The results presented here represent a first step towards the elucidation of the pathway of events leading from growth factor-receptor interaction to this induction. A series of Bal 31 deletions of the human vimentin promoter are used to show that a sequence residing at -700 is responsible for the serum, and also TPA inducibility of this gene. This sequence is able to confer serum inducibility upon uninducible constructs regardless of its position and orientation, indicating that it is this element alone which is required for this induction. The isolated sequence is a strong enhancer as well. Further deletions and the use of synthetic oligonucleotides demonstrate that a 24-mer containing two AP-1/jun binding sites confer both serum and TPA inducibility upon the human vimentin gene. Gel retardation analysis confirms that this sequence binds an AP-1 -like protein.

MeSH terms

  • Animals
  • Base Sequence
  • Binding Sites
  • Blood
  • Cells, Cultured
  • Chromosome Deletion
  • Culture Media
  • Enhancer Elements, Genetic
  • Gene Expression Regulation*
  • Genes* / drug effects
  • Humans
  • Insulin-Like Growth Factor I / genetics
  • Metallothionein / genetics
  • Mice
  • Mice, Inbred BALB C
  • Molecular Sequence Data
  • Promoter Regions, Genetic*
  • RNA, Messenger / genetics
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription, Genetic
  • Transfection
  • Vimentin / biosynthesis
  • Vimentin / genetics*

Substances

  • Culture Media
  • RNA, Messenger
  • Vimentin
  • Insulin-Like Growth Factor I
  • Metallothionein
  • Tetradecanoylphorbol Acetate