Document 1131
 DOCN  M9591131
 TI    Role of the hepatitis B virus posttranscriptional regulatory element in
       export of intronless transcripts.
 DT    9509
 AU    Huang ZM; Yen TS; Department of Pathology, University of California, San
       Francisco,; USA.
 SO    Mol Cell Biol. 1995 Jul;15(7):3864-9. Unique Identifier : AIDSLINE
       MED/95311986
 AB    Hepatitis B virus S transcripts contain a region, known as the
       posttranscriptional regulatory element (PRE), that activates their
       transport from the nucleus to the cytoplasm. J. Huang and T. J. Liang
       (Mol. Cell. Biol. 13:7476-7486, 1993) have shown that this element can
       partially substitute for the human immunodeficiency virus Rev-response
       element (RRE) in a reporter plasmid that is dependent on the RRE and Rev
       protein for expression and concluded that PRE exhibits Rev-RRE-like
       functions by inhibiting splicing. However, we have obtained additional
       data which indicate that the PRE functions in a novel manner that is not
       dependent on inhibition of splicing. Unlike Rev-RRE, the PRE functions
       independently of splice donor and acceptor sites and can activate
       cytoplasmic expression of an intronless (so-called prespliced)
       beta-globin transcript. Conversely, a heterologous intron can substitute
       for the PRE in increasing cytoplasmic expression of hepatitis B virus S
       transcripts. In addition, the host nuclear factor, YL2 (p32), which
       enhances Rev-RRE function has no effect on PRE-dependent gene
       expression. Since S transcripts are not normally known to be spliced and
       since RNA splicing and cytoplasmic transport are tightly linked
       processes in higher eucaryotic cells, we conclude that the PRE functions
       in cis to allow the export of nuclear transcripts that do not interact
       efficiently with the splicing pathway and hence are normally not
       exported well from the nucleus. Such elements are critical for the life
       cycle of viruses, such as hepatitis B virus, which undergo reverse
       transcription during replication.
 DE    Base Sequence  Biological Transport  Cell Compartmentation  Cell
       Nucleus/METABOLISM  Cytoplasm/METABOLISM  Gene Products, rev/METABOLISM
       Globin/BIOSYNTHESIS/GENETICS  Hepatitis B Surface Antigens/BIOSYNTHESIS
       Hepatitis B Virus/*GENETICS  Introns/*GENETICS  Molecular Sequence Data
       Regulatory Sequences, Nucleic Acid/*GENETICS  *RNA Processing,
       Post-Transcriptional  RNA Splicing/GENETICS  RNA, Messenger/*METABOLISM
       RNA, Viral/*METABOLISM  Support, U.S. Gov't, Non-P.H.S.  Support, U.S.
       Gov't, P.H.S.  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).