Previous Article | Next Article ![]()
Journal of Virology, July 2000, p. 6039-6044, Vol. 74, No. 13
Howard Hughes Medical Institute, Departments
of Medicine and Microbiology and Immunology, University of
California, San Francisco, California 94143-0703
Received 21 January 2000/Accepted 4 April 2000
Transcriptional transactivators (Tat) from many lentiviruses
interact with their cognate transactivation response RNA structures (TAR) to increase rates of elongation rather than initiation of transcription. For several of them, the complex of Tat and a
species-specific cyclin T1 must be formed before the binding to TAR can
occur with high affinity and specificity. In sharp contrast, Tat from
the bovine immunodeficiency virus (BIV) binds to its TAR without the help of the cyclin T1. This binding depends on the upper stem and 5'
bulge, but not the central loop in TAR. Moreover, cyclins T1 from
different species can mediate effects of this Tat in cells. Unlike the
situation with other lentiviruses, Tat transactivation can be rescued
simply by linking a heterologous promoter to TAR in permissive cells.
Thus, lentiviruses have evolved different strategies to recruit Tat and
the positive transcription elongation factor b to their promoters, and
interactions between Tat and TAR are independent from those between Tat
and the cyclin T1 in BIV.
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Binding of Tat to TAR and Recruitment of Positive Transcription
Elongation Factor b Occur Independently in Bovine
Immunodeficiency Virus
*
Corresponding author. Mailing address: Room N215,
UCSF-Mt. Zion Cancer Center, 2340 Sutter St., San Francisco, CA 94115. Phone: (415) 502-1905. Fax: (415) 502-1901. E-mail:
matija{at}itsa.ucsf.edu.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»