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Journal of Virology, March 2009, p. 2265-2273, Vol. 83, No. 5
0022-538X/09/$08.00+0     doi:10.1128/JVI.01785-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

ORF30 and ORF34 Are Essential for Expression of Late Genes in Murine Gammaherpesvirus 68{triangledown}

Ting-Ting Wu,1,2* Tina Park,3 Hana Kim,4 Thuy Tran,1 Leming Tong,1 DeeAnn Martinez-Guzman,5 Nichole Reyes,1,{dagger} Hongyu Deng,2,6 and Ren Sun1,2,5

Department of Molecular and Medical Pharmacology,1 Dental Research Institute, School of Dentistry,2 Department of Molecular Cell and Developmental Biology,3 Department of Psychobiology,4 Molecular Biology Institute, University of California at Los Angeles, Los Angeles, California 90095,5 Center for Infection and Immunity, National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, People's Republic of China6

Received 25 August 2008/ Accepted 9 December 2008

A hallmark of productive infection by DNA viruses is the coupling of viral late gene expression to genome replication. Here we report the identification of open reading frame 30 (ORF30) and ORF34 as viral trans factors crucial for activating late gene transcription following viral DNA replication during lytic infection of murine gammaherpesvirus 68 (MHV-68). The mutant virus lacking either ORF30 or ORF34 underwent normal DNA replication but failed to express viral late gene transcripts, leading to nonproductive infection. In a reporter assay system, ORF30 and ORF34 were required for MHV-68 to activate the viral late gene promoters. Furthermore, studies using chromatin immunoprecipitation assays showed that the recruitment of RNA polymerase II to the viral late promoters during lytic infection was significantly reduced in the absence of ORF30 or ORF34. Together, the results suggest that ORF30 and ORF34 may play an important role in the assembly of the transcription initiation complex at the late gene promoters. Our discovery of the viral mutants that uncouple late gene transcription from DNA replication lays an important foundation to dissect the mechanism of this critical step of gene expression regulation.

* Corresponding author. Mailing address: 650 Charles E. Young Drive, CHS 23-120, University of California at Los Angeles, Los Angeles, CA 90095. Phone: (310) 267-2218. Fax: (310) 825-6267. E-mail: twu{at}mednet.ucla.edu

{triangledown} Published ahead of print on 17 December 2008.

{dagger} Present address: University of California at San Francisco, San Francisco, CA 94143.

Journal of Virology, March 2009, p. 2265-2273, Vol. 83, No. 5
0022-538X/09/$08.00+0     doi:10.1128/JVI.01785-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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