HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Devireddy, L. R. Articles by Jones, C. J. Search for Related Content PubMed PubMed Citation Articles by Devireddy, L. R. Articles by Jones, C. J. Social Bookmarking                      What's this?

J Biol Chem, Vol. 275, Issue 1, 77-81, January 7, 2000

Olf-1, a Neuron-specific Transcription Factor, Can Activate the Herpes Simplex Virus Type 1-Infected Cell Protein 0 Promoter^*

Laxminarayana R. Devireddy and Clinton J. Jones^§

From the Center for Biotechnology, Department of Veterinary and Biomedical Sciences, University of Nebraska, Lincoln, Nebraska 68583-0905

Herpes simplex virus type 1 (HSV-1) establishes a life-long latent infection in sensory neurons of infected individuals. Infected cell protein 0 (ICP0) is important for productive infection and reactivation from latency. Thus, activation of ICP0 expression in neurons is likely to be important for reactivation from latency. In a mouse neuroblastoma cell line, ICP0 promoter activity is high compared with other strong viral promoters. In contrast, promoter activity is low in non-neuronal cells. DNase I footprinting assays indicated that three distinct motifs in the ICP0 promoter are bound by nuclear factors. One of these motifs contains a binding site for a novel helix-loop-helix olfactory neuron-specific transcription factor (Olf-1). Gel shift assays and supershift assays using an Olf-1-specific antibody demonstrated that mouse neuroblastoma cells express Olf-1, which is bound to the Olf-1-like site in the ICP0 promoter. Deletion of the putative Olf-1 motif reduced ICP0 promoter activity more than 5-fold in mouse neuroblastoma cells and prevented trans-activation by an Olf-1 expression vector. We hypothesize that the Olf-1-binding site activates ICP0 promoter activity in neurons during reactivation from latency.

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				R. L. Thompson, M. T. Shieh, and N. M. Sawtell Analysis of Herpes Simplex Virus ICP0 Promoter Function in Sensory Neurons during Acute Infection, Establishment of Latency, and Reactivation In Vivo J. Virol., November 15, 2003; 77(22): 12319 - 12330. [Abstract] [Full Text] [PDF]

				V. Geiser and C. Jones Stimulation of bovine herpesvirus-1 productive infection by the adenovirus E1A gene and a cell cycle regulatory gene, E2F-4 J. Gen. Virol., April 1, 2003; 84(4): 929 - 938. [Abstract] [Full Text] [PDF]

				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]

				C. M. Loiacono, R. Myers, and W. J. Mitchell Neurons Differentially Activate the Herpes Simplex Virus Type 1 Immediate-Early Gene ICP0 and ICP27 Promoters in Transgenic Mice J. Virol., March 1, 2002; 76(5): 2449 - 2459. [Abstract] [Full Text] [PDF]

				M. Inman, G.-C. Perng, G. Henderson, H. Ghiasi, A. B. Nesburn, S. L. Wechsler, and C. Jones Region of Herpes Simplex Virus Type 1 Latency-Associated Transcript Sufficient for Wild-Type Spontaneous Reactivation Promotes Cell Survival in Tissue Culture J. Virol., April 15, 2001; 75(8): 3636 - 3646. [Abstract] [Full Text]

				M. Inman, Y. Zhang, V. Geiser, and C. Jones The zinc ring finger in the bICP0 protein encoded by bovine herpesvirus-1 mediates toxicity and activates productive infection J. Gen. Virol., March 1, 2001; 82(3): 483 - 492. [Abstract] [Full Text]