DEFECTIVE TRANSCRIPTIONAL ACTIVATION BY DIVERSE VP16 MUTANTS ASSOCIATED WITH A COMMON INABILITY TO FORM OPEN PROMOTER COMPLEXES

Three different types of VP16 mutants were assayed in vitro. These inc luded deletion of the C-terminal activation subdomain and alterations in either the acidic or non-acidic components of the minimal activatio n domain. The mutant GAL4-VP16 proteins were found to be transcription ally defective using a HeLa cell nuclear extract. In all three cases t he loss of transcription activity was accompanied by a commensurate lo ss in ability to form open transcription complexes. The comparison imp lies that the diverse components of GAL4-VP16 activate transcription b y the common facilitation of steps required for open complex formation . The results further imply that open complex formation may be a commo n target for mammalian transcriptional activation, as known previously to be the case in bacterial systems.