Skip Navigation

This Article
Right arrow Print PDF (1446K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Latchman, D.S.
Right arrow Articles by Kemp, L.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Latchman, D.S.
Right arrow Articles by Kemp, L.M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1989, Vol. 17, No. 21 8533-8542
© 1989


MOLECULAR BIOLOGY

The different competitive abilities of viral TAATGARAT elements and cellular octamer motifs, mediate the induction of viral immediate-early genes and the repression of the histone H2B gene in herpes simplex virus infected cells

D.S. Latchman*, J.F. Pratridge and L.M. Kemp

Medical Molecular Biology Unit, Department of Biochemistry, University College and Middlesex School of Medicine The Windeyer Building, Cleveland Street, London W1P 6DB, UK

*To whom correspondence should be addressed

Received August 1, 1989. Revised September 18, 1989. Accepted September 18, 1989.

An HSV virion component, Vmw65, interacts with cellular transcription factors to transactivate TAATGARAT-containing viral genes and some cellular genes containing the related octamer element. We show that the octamer-containing histone H2B promoter can be trans-activated by transfection of Vmw65 but not by viral infection. The induction of H2B transcription by Vmw65 can be abolished by co-transfection of excess amounts of either a TAATGARAT element or a Vmw65 responsive octamer element. This effect cannot be overcome by addition of increasing amounts of Vmw65. The H2B promoter and TAATGARAT-containing viral promoters therefore compete for limiting cellular factors required for induction by Vmw65 resulting in repression of the H2B gene during lytic infection. The competitive effect of TAATGARAT elements on the H2B gene is not observed in the absence of Vmw65, but can be produced in the presence of a truncated form of Vmw65 lacking the acidic tail required for transcriptional activation. Hence a domain of Vmw65 distinct from that involved in transcriptional induction interacts with cellular octamer binding proteins favouring binding to the TAATGARAT motif.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Clin. Microbiol. Rev.Home page
C. Jones
Herpes Simplex Virus Type 1 and Bovine Herpesvirus 1 Latency
Clin. Microbiol. Rev., January 1, 2003; 16(1): 79 - 95.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.