Tat-dependent occlusion of the HIV poly(A) site

Caroline Weichs An Der Glon, Mark Ashe, Jan Eggermont, Nick J. Proudfoot

    Research output: Contribution to journalArticlepeer-review


    Retroviruses must ensure that poly(A) signals in the 3′89 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 sequences in the 3′ LTR may contribute to this regulation. We have discovered a novel regulatory mechanism for poly(A) site occlusion in HIV-1. When transcription initiation from the HIV promoter is activated by Tat, the HIV poly(A) site is specifically occluded, while other poly(A) sites are unaffected by Tat. Nucleotide signals associated with this Tat effect are immediately adjacent to the AAUAAA sequence of the HIV-1 poly(A) signal. These data suggest that elongating RNA polymerase II, activated by Tat specifically occludes the HIV poly(A) site.
    Original languageEnglish
    Pages (from-to)2119-2128
    Number of pages9
    JournalEMBO Journal
    Issue number5
    Publication statusPublished - 1993


    • HIV-1
    • Poly(A) site occlusion
    • RNA polymerase II
    • Tat


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