       Document 0532
 DOCN  M9630532
 TI    High-resolution mapping of the human T-cell leukemia virus type 1
       Rex-binding element by in vitro selection.
 DT    9603
 AU    Baskerville S; Zapp M; Ellington AD; Department of Chemistry and
       Microbiology, Indiana University,; Bloomington 47405, USA.
 SO    J Virol. 1995 Dec;69(12):7559-69. Unique Identifier : AIDSLINE
       MED/96078999
 AB    Interactions between the Rex protein of HTLV-1 and the genomic
       Rex-binding element (XBE) mediate the cytoplasmic transport of viral
       mRNAs. However, it is uncertain which RNA sequences and structures
       contribute to Rex recognition. A portion of the viral genome that
       spanned the XBE was partially randomized, and functional Rex-binding
       variants were selected. Alignment of selected Rex-binding sequences
       revealed positions that were functionally conserved between different
       molecules. A model is presented in which a subset of the selected
       residues are in direct contact with Rex. Positions that covaried with
       one another were also found. These covariations support a
       secondary-structural model in which a central paired stem is
       symmetrically flanked by two bulge loops. On the basis of this model,
       site-directed mutations of the XBE were constructed and each half
       molecule was found to bind independently to Rex. The functional residues
       and secondary structures in the XBE half molecules bear a remarkable
       resemblance to the transactivation response region element of HIV-1.
       Since the transactivation response region element is known to interact
       specifically with arginine residues in the Tat protein, these results
       suggest that the XBE binds to the arginine-rich RNA-binding domain of
       Rex in a similar manner. This model is supported by the selection data.
 DE    Base Composition  Base Sequence  Binding Sites  Cloning, Molecular
       Conserved Sequence  Gene Products, rex/BIOSYNTHESIS/*METABOLISM  Human
       HTLV-I/*METABOLISM  Molecular Sequence Data  Mutagenesis, Site-Directed
       Nucleic Acid Conformation  Oligodeoxyribonucleotides  Random Allocation
       Recombinant Fusion Proteins/BIOSYNTHESIS/METABOLISM  RNA,
       Messenger/*CHEMISTRY/*METABOLISM  RNA, Viral/CHEMISTRY/*METABOLISM
       Support, Non-U.S. Gov't  Support, U.S. Gov't, Non-P.H.S.  Support, U.S.
       Gov't, P.H.S.  Variation (Genetics)  JOURNAL ARTICLE

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

