F. Kashanchi et al., INVOLVEMENT OF TRANSCRIPTION FACTOR YB-1 IN HUMAN T-CELL LYMPHOTROPICVIRUS TYPE-I BASAL GENE-EXPRESSION, Journal of virology, 68(1), 1994, pp. 561-565
Sequences which control basal human T-cell lymphotropic virus type I (
HTLV I) transcription likely play an important role in initiation and
maintenance of virus replication. We previously identified and analyze
d a 45-nucleotide sequence (downstream regulatory element 1 [DRE 1]),
+195 to +240, at the boundary of the R/U5 region of the long terminal
repeat which is required for HTLV-I basal transcription. We identified
a protein, p37, which specifically bound to DRE 1. An affinity column
fraction, containing p37, stimulated HTLV-I transcription approximate
ly 12-fold in vitro. We now report the identification of a cDNA clone
(15B-7), from a Jurkat expression library, that binds specifically to
the DRE 1 regulatory sequence. Binding of the cDNA fusion protein, sim
ilarly to the results obtained with purified Jurkat protein, was decre
ased by introduction of site-specific mutations in the DRE 1 regulator
y sequence. In vitro transcription and translation of 15B-7 cDNA produ
ced a fusion protein which bound specifically to the HTLV-I +195 to +2
40 oligonucleotide. The partial cDNA encodes a protein which is homolo
gous to the C-terminal 196 amino acids of the 36-kDa transcription fac
tor, YB-1. Cotransfection of a YB-1 expression plasmid increases HTLV-
I basal transcription approximately 14-fold in Jurkat T lymphocytes. O
n the basis of the molecular weight, DNA-binding characteristics, and
in vivo transactivation activity, we suggest that the previously ident
ified DRE 1-binding protein, p37, is YB-1.