Nucleic Acids Research, Vol 24, Issue 4 549-557, Copyright © 1996 by Oxford University Press
RD Williams, BA Lee, SP Jackson and NJ Proudfoot
Transcription from a minimal HIV-1 promoter containing the three Sp1
binding sites and TATA box can be activated without Tat by template DNA
replication. Here we show that this activation can also be mediated by
recombinant GAL4 fusion proteins containing the activation domains of Sp1,
VP16 or CTF (or by full-length GAL4) targeted to the HIV-1 promoter by
replacing the Sp1 sites with five GAL4 binding sites. Thus Sp1 is not
unique in its ability to mediate replication activated transcription,
although the degree of processivity elicited by the different activators
varied significantly from strongly processive (GAL4-VP16) to relatively
non-processive (GAL4-Sp1 or -CTF). Processive GAL4-VP16-activated
transcription, but not efficient initiation, required multiple GAL4 binding
sites. In the presence of Tat, transcription with GAL4-SP1 and GAL4-CTF was
further activated (principally at the level of processivity) but
GAL4-VP16-potentiated transcription was only slightly stimulated. The
Tat-dependent switch from non-processive to fully processive transcription
was particularly marked for GAL4-Sp1, an effect which may be relevant to
the selection of Sp1 binding sites by the HIV-1 promoter.
ARTICLES
Activation domains of transcription factors mediate replication dependent transcription from a minimal HIV-1 promoter
Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.
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