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Document 1063
DOCN M9471063
TI HTLV-I LTR 21 bp repeat-specific and neuroglial cell-specific
DNA-protein complexes (Meeting abstract).
DT 9409
AU Tillmann M; Hinkel R; Wigdahl B; Dept. of Microbiology and Immunology,
Pennsylvania State Univ.; Coll. of Medicine, Hershey, PA
SO International Association for Comparative Research on Leukemia and
Related Diseases, 16th Symposium. July 11-16, 1993, Montreal, Quebec,
Canada, A54, 1993.. Unique Identifier : AIDSLINE ICDB/94698652
AB Human T-cell leukemia virus type I (HTLV-I) is an etiologic agent of
adult T-cell leukemia and a chronic neurologic disorder, tropical
spastic paraparesis. An HTLV-I-encoded protein, Tax, is capable of
transcriptionally trans-activating HTLV-I by interacting with specific
sequences in the HTLV-I long terminal repeat (LTR) which comprise an
inducible enhancer containing three imperfect tandem repeats of a 21 bp
sequence. Evidence suggests that Tax is incapable of directly
interacting with DNA; therefore, Tax most likely regulates transcription
via interaction with cellular factors. Characterization of the cellular
factors which interact with the 21 bp repeats is essential to
understanding the molecular mechanisms involved in Tax-mediated
trans-activation as well as the involvement of Tax and the LTR in the
cellular tropism of HTLV-I. Utilizing the electrophoretic mobility shift
assay (EMSA), we detect both 21 bp repeat-specific and neuroglial
cell-specific DNA-protein complexes. When nuclear extracts derived from
cells of lymphoid (Jurkat), monocytoid (U937), neuronal (IMR-32), and
glial (U-373 MG) cell origin are reacted with each of the three 21 bp
repeats, several 21 bp repeat-specific DNA-protein complexes are
detected. Results from EMSA competition analyses utilizing unlabeled 21
bp repeats as competitor DNAs indicate a difference in the ability of
each unlabeled 21 bp repeat to compete for the specific DNA-protein
complexes formed between the nuclear extracts and each of the
radiolabeled 21 bp repeats. In each case, the most effective competitor
is the homologous, unlabeled 21 bp repeat. Additional results from EMSA
competition assays utilizing oligonucleotides containing the consensus
sequence for CRE, Ap-2, NF-kappa B, or Sp1 demonstrate that, of the
specific DNA-protein complexes, there is differential competition for
complex formation with each of the three 21 bp repeats. These studies
indicate that each of the three 21 bp Tax-responsive elements may be
unique with respect to their participation in specific DNA-protein
complex formation. In addition to detecting 21 bp repeat-specific
DNA-protein complexes, neuroglial cell type-specific DNA-protein
complexes are also detected. A unique DNA-protein complex is detected
when nuclear extracts derived from IMR-32 and U373-MG cells are reacted
with the middle 21 bp repeat. Furthermore, one of the specific
DNA-protein complexes detected when the nuclear extracts derived from
Jurkat, U937, and IMR-32 cell lines are reacted with each of the three
21 bp repeats is not detected when nuclear extracts derived from U-373
MG cells are reacted with each of the three 21 bp repeats.
Characterization of the 21 bp repeat-specific and neuroglial
cell-specific DNA-protein complexes is currently under investigation.
DE Amino Acid Sequence DNA/*ANALYSIS DNA-Binding Proteins/GENETICS Gene
Products, tax/GENETICS HIV Enhancer HIV Long Terminal Repeat/*GENETICS
HTLV-I/*GENETICS Human NF-kappa B/GENETICS
Neuroglia/CYTOLOGY/METABOLISM Trans-Activation (Genetics) MEETING
ABSTRACT
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).