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 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.
Sir William Dunn School of Pathology, Oxford, UK.
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Weichs an der Glon
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Eggermont
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Proudfoot
D001483:Base Sequence; D004279:DNA, Viral; D015696:Gene Products, tat / Q000378:metabolism*; D006678:HIV / Q000235:genetics / Q000378:metabolism*; D016325:HIV Long Terminal Repeat; D006367:HeLa Cells; D006801:Humans; D008969:Molecular Sequence Data; D011061:Poly A / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D012689:Sequence Homology, Nucleic Acid; D015533:Transcriptional Activation; D054322:tat Gene Products, Human Immunodeficiency Virus
D004279:DNA, Viral; D015696:Gene Products, tat; D054322:tat Gene Products, Human Immunodeficiency Virus; D011061:Poly A