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 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.
Jiang
Y
Y
Department of Chemistry and Biochemistry, University of California, Los Angeles 90024.
Triezenberg
S J
SJ
Gralla
J D
JD
D005656:Fungal Proteins / Q000235:genetics*; D006367:HeLa Cells; D006801:Humans; D009154:Mutation; D011401:Promoter Regions, Genetic; D015534:Trans-Activators / Q000235:genetics*; D015533:Transcriptional Activation
D005656:Fungal Proteins; C070633:Gal-VP16; D015534:Trans-Activators