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M9460581.TXT
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1994-06-25
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Document 0581
DOCN M9460581
TI Cellular and viral specificity of equine infectious anemia virus Tat
transactivation.
DT 9408
AU Maury WJ; Carpenter S; Graves K; Chesebro B; LPVD, Rocky Mountain
Laboratories, NIAID, Hamilton, Montana; 59840.
SO Virology. 1994 May 1;200(2):632-42. Unique Identifier : AIDSLINE
MED/94233726
AB Lentiviruses vary in their dependence on a functional tat gene during
their viral life cycle. To begin to understand the viral and cellular
parameters controlling equine infectious anemia virus (EIAV)
transactivation, we investigated Tat function and Tat and LTR structural
requirements necessary for successful transactivation. EIAV Tat
expression was required for detection of viral antigens from a
full-length provirus. The level of transactivation by EIAV Tat as
measured by LTR-CAT assays correlated well with viral antigen
expression. Using horse/mouse somatic cell hybrids (SCH), a single SCH
line which supported EIAV transactivation was identified, indicating
that the presence of specific horse chromosomes provided cellular
factors required for transactivation. Transformed cell lines from
several different species were also tested and found to differ in their
ability to support EIAV transactivation. A canine cell line, Cf2Th,
which was permissive for EIAV transactivation, and a human cell line,
HeLa, which was not permissive for EIAV transactivation, were used to
map regions of the LTR and Tat that were important in cell-specific
transactivation. As expected, the R region of EIAV LTR was required for
transactivation by EIAV Tat in all cell lines studied. Similarly, the R
region of HIV LTR was necessary for transactivation by HIV Tat. However,
the composition of the U3 region also influenced transactivation in a
cell-specific manner. In Cf2Th cells, replacement of EIAV U3 sequences
with HIV U3 sequences resulted in high basal (nontransactivated)
expression, and as a result, only a twofold increase in expression was
observed in the presence of EIAV Tat. Similar studies using HIV Tat
demonstrated that transactivation occurred in Cf2Th cells when either
EIAV or HIV U3 sequences were present in the LTR. In contrast,
transactivation by either HIV or EIAV Tat in HeLa cells required the
presence of HIV enhancer sequences. These findings suggested that the
ability of transactivation to occur in some cell lines may involve
interactions between cell-specific transcription factors and the
activation domain of Tat. For transactivation in other cell lines, Tat
appeared to require more ubiquitious factors that interact with both
EIAV and HIV U3 sequences.
DE Animal Antigens, Viral/BIOSYNTHESIS Base Sequence Cell Line Chimeric
Proteins/METABOLISM Comparative Study Enhancer Elements
(Genetics)/GENETICS Gene Expression Regulation, Viral Gene Products,
tat/GENETICS/*METABOLISM Genes, tat/*GENETICS Horses Human Hybrid
Cells Infectious Anemia Virus, Equine/*GENETICS Mice Molecular
Sequence Data Proviruses/GENETICS Repetitive Sequences, Nucleic
Acid/GENETICS Species Specificity Support, U.S. Gov't, P.H.S.
*Trans-Activation (Genetics) Transcription Factors/GENETICS/*METABOLISM
JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).