title: Defective transcriptional activation by diverse VP16 mutants associated with a common inability to form open promoter complexes.
abstract: Three different types of VP16 mutants were assayed in vitro. These included deletion of the C-terminal activation subdomain and alterations in either the acidic or non-acidic components of the minimal activation domain. The mutant GAL4-VP16 proteins were found to be transcriptionally defective using a HeLa cell nuclear extract. In all three cases the loss of transcription activity was accompanied by a commensurate loss in ability to form open transcription complexes. The comparison implies that the diverse components of GAL4-VP16 activate transcription by the common facilitation of steps required for open complex formation. The results further imply that open complex formation may be a common target for mammalian transcriptional activation, as known previously to be the case in bacterial systems.
authors.affiliation: Department of Chemistry and Biochemistry, University of California, Los Angeles 90024.
authors.forename: Y
authors.initials: Y
authors.lastname: Jiang
authors.forename: S J
authors.initials: SJ
authors.lastname: Triezenberg
authors.forename: J D
authors.initials: JD
authors.lastname: Gralla
mesh_terms: D005656:Fungal Proteins / Q000235:genetics*; D006367:HeLa Cells; D006801:Humans; D009154:Mutation; D011401:Promoter Regions, Genetic; D015534:Trans-Activators / Q000235:genetics*; D015533:Transcriptional Activation
chemical_list: D005656:Fungal Proteins; C070633:Gal-VP16; D015534:Trans-Activators