NF-KAPPA-B HOMODIMER BINDING WITHIN THE HIV-1 INITIATOR REGION AND INTERACTIONS WITH TFII-I

We show that the binding of Rel p50 and p52 homodimers at sites within the transcriptional initiation region of HIV-1 provides for their abi lity to interact with other proteins that bind the initiator. The bind ing of one such protein, the initiator protein TFII-I, to the initiati on region of HIV-1 is augmented in the presence of Rel p50 and Rel p52 homodimers. Consistent with this, in vitro Rel homodimers potentiate HIV-1 transcription in a manner dependent upon TFII-I. The findings su ggest that Rel dimers may regulate HIV-1 transcription in two ways. Fi rst, through binding at the kappa B enhancer sites at (-104 to -80), N F-kappa B p50:p65 participates in classical transcriptional activation . Second, Rel dimers such as p50 or p52 might bind at initiator sequen ces to regulate the de novo binding of components of certain preinitia tion complexes. These findings, and the existence of Rel binding sites at the initiators of other genes, suggest roles for Rel proteins in e arly events determining transcriptional control.