This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Quadt, I.
Right arrow Articles by Knebel-Mörsdorf, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Quadt, I.
Right arrow Articles by Knebel-Mörsdorf, D.

 Previous Article  |  Next Article 

Journal of Virology, June 2007, p. 6122-6127, Vol. 81, No. 11
0022-538X/07/$08.00+0     doi:10.1128/JVI.02768-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Studies of the Silencing of Baculovirus DNA Binding Protein{triangledown}

Ilja Quadt,1,2 Jan W. M. van Lent,3 and Dagmar Knebel-Mörsdorf1,2*

Department of Neurology,1 Center for Biochemistry, University of Cologne, D-50931 Cologne, Germany,2 Laboratory of Virology, Department of Plant Sciences, Wageningen University, 6709 PD Wageningen, The Netherlands3

Received 15 December 2006/ Accepted 9 March 2007

Baculovirus DNA binding protein (DBP) binds preferentially single-stranded DNA in vitro and colocalizes with viral DNA replication sites. Here, its putative role as viral replication factor has been addressed by RNA interference. Silencing of DBP in Autographa californica multiple nucleopolyhedrovirus-infected cells increased expression of LEF-3, LEF-4, and P35. In contrast, expression of the structural genes coding for P39 and polyhedrin was suppressed while expression of genes coding for P10 and GP64 was unaffected. In the absence of DBP, viral DNA replication sites were formed, indicating replication of viral DNA. Electron microscopy studies, however, revealed a loss of formation of polyhedra and virus envelopment, suggesting that the primary role of DBP is viral formation rather than viral DNA replication.


* Corresponding author. Mailing address: Department of Neurology and Center for Biochemistry, Joseph-Stelzmann-Strasse 52, D-50931 Köln, Germany. Phone: 49-221-47886694. Fax: 49-221-4786977. E-mail: dagmar.moersdorf{at}uni-koeln.de

{triangledown} Published ahead of print on 21 March 2007.


Journal of Virology, June 2007, p. 6122-6127, Vol. 81, No. 11
0022-538X/07/$08.00+0     doi:10.1128/JVI.02768-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Schultz, K. L. W., Wetter, J. A., Fiore, D. C., Friesen, P. D. (2009). Transactivator IE1 Is Required for Baculovirus Early Replication Events That Trigger Apoptosis in Permissive and Nonpermissive Cells. J. Virol. 83: 262-272 [Abstract] [Full Text]  
  • Yu, Q., Lin, T., Feng, G., Yang, K., Pang, Y. (2008). Functional analysis of the putative antiapoptotic genes, p49 and iap4, of Spodoptera litura nucleopolyhedrovirus with RNAi. J. Gen. Virol. 89: 1873-1880 [Abstract] [Full Text]