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Nucleic Acids Research, 1993, Vol. 21, No. 8 1959-1964
© 1993

MOLECULAR BIOLOGY

The transcriptional enhancer element, xB, regulates promoter activity of the human neurotropic virus, JCV, in cells derived from the CNS

Perungavur N. Ranganathan and Kamel Khalili*

Molecular Neurovirology Section, Jefferson Institute of Molecular Medicine, Department of Biochemistry and Molecular Biology, Thomas Jefferson University Philadelphia, PA 19107, USA

* To whom correspondence should be addressed

Received November 6, 1992. Revised March 16, 1993. Accepted March 16, 1993.

Studies on the regulation of the human neurotropic virus (JCV) promoter, have been focused primarily on the 98 bp tandem repeat sequence which confers gllal-speciflclty to viral gene expression. We demonstrate that a distinct regulatory element outside of the 98 bp region, which spans a stretch of 10 nucleotides (nt) (5'-GGGAATTTCC-3') Increases transcrlptional activity of JCV late (JCVL) and early (JCVE) promoters in glial cells. Sequence analysis of this motif reveals extensive homology to the xB sequence of HIV-1 (5'-GGGACTT-TCC-3'). A DNA fragment corresponding to the 10 nt sequence of JCV exhibits transcrlptional activity when placed upstream of the test promoter in glial cells. The induction mediated by this regulatory motif Is moderately enhanced in response to phorbol 12-myrls-tate 13-acetate (PMA) in glial cells. Band-shift and UV-crosslinklng experiments suggest that glial cells constitutively produce proteins that specifically interact with the JCV xB, but not the HIV-1 xB motif. Treatment of cells with PMA results in formation of new complexes that are sensitive to the xB sequences derived from the JCV and HIV-1 genomes. These results suggest that the xB sequence located in the JCV genome may play a role in transcriptional regulation of JCV gene expression by interacting with inducible and uninducible nuclear proteins from glial cells.


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