The acidic transcriptional activator GAL-VP16 acts on preformed template-committed complexes

EMBO J. 1992 Jun;11(6):2229-40. doi: 10.1002/j.1460-2075.1992.tb05282.x.

Abstract

The action of the chimeric acidic transcriptional activator GAL-VP16 has been investigated by performing a series of kinetic experiments using the detergent Sarkosyl as well as monoclonal antibodies which specifically inhibit GAL-VP16 DNA binding and transcriptional activation. GAL-VP16 binds to recognition site rapidly, remains bound after transcriptional initiation and is required to maintain stimulated levels of reinitiation. GAL-VP16 action, which appears to result in an increase in the number of preinitiation complexes formed, occurs after the formation of template-committed complexes composed of promoter-bound TFIIA (STF) and a partially purified TFIID fraction conferring GAL-VP16 responsiveness on a reconstituted basal transcription system. This TFIID fraction cannot be replaced by TFIIB or cloned TFIID. Our results suggest that GAL-VP16 activates step(s) in preinitiation complex assembly occurring after TFIID has bound.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Monoclonal
  • Base Sequence
  • Binding Sites
  • Chimera
  • Epitopes / analysis
  • Fungal Proteins / analysis
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism*
  • HeLa Cells
  • Humans
  • Kinetics
  • Molecular Sequence Data
  • Oligodeoxyribonucleotides
  • Restriction Mapping
  • Sarcosine / analogs & derivatives
  • Sarcosine / pharmacology
  • Templates, Genetic
  • Trans-Activators / analysis
  • Trans-Activators / genetics
  • Trans-Activators / metabolism*
  • Transcription, Genetic* / drug effects

Substances

  • Antibodies, Monoclonal
  • Epitopes
  • Fungal Proteins
  • Gal-VP16
  • Oligodeoxyribonucleotides
  • Trans-Activators
  • sarkosyl
  • Sarcosine