TAT-DEPENDENT OCCLUSION OF THE HIV POLY(A) SITE

Retroviruses must ensure that poly(A) signals in the 3' LTR are highly active, while identical signals in the 5' LTR are inactive (occluded) . In the case of HIV-1, both promoter proximity in the 5' LTR and U3 s equences in the 3' LTR may contribute to this regulation. We have disc overed a novel regulatory mechanism for poly(A) site occlusion in HIV- 1. When transcription initiation from the B[tV promoter is activated b y Tat, the HIV poly(A) site is specifically occluded, while other poly (A) sites are unaffected by Tat. Nucleotide signals associated with th is Tat effect are immediately adjacent to the AAUAAA sequence of the H IV-1 poly(A) signal. These data suggest that elongating RNA polymerase II, activated by Tat specifically occludes the HIV poly(A) site.