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 Ahmed, M.
Right arrow Articles by Lyles, D. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ahmed, M.
Right arrow Articles by Lyles, D. S.

 Previous Article  |  Next Article 

Journal of Virology, October 1998, p. 8413-8419, Vol. 72, No. 10
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Effect of Vesicular Stomatitis Virus Matrix Protein on Transcription Directed by Host RNA Polymerases I, II, and III

Maryam Ahmed and Douglas S. Lyles*

Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157

Received 6 April 1998/Accepted 16 June 1998

The matrix (M) protein of vesicular stomatitis virus (VSV) functions in virus assembly and inhibits host-directed gene expression independently of other viral components. Experiments in this study were carried out to determine the ability of M protein to inhibit transcription directed by each of the three host RNA polymerases (RNA polymerase I [RNAPI], RNAPII, and RNAPIII). The effects of wild-type (wt) VSV, v6 (a VSV mutant isolated from persistently infected cells), and tsO82 viruses on poly(A)+ and poly(A)- RNA synthesis were measured by incorporation of [3H]uridine. v6 and tsO82 viruses, which contain M-gene mutations, had a decreased ability to inhibit synthesis of both poly(A)+ and poly(A)- RNA. Nuclear runoff analysis showed that VSV inhibited transcription of 18S rRNA and alpha -tubulin genes, which was dependent on RNAPI and RNAPII, respectively, but infection with wt virus enhanced transcription of 5S rRNA by RNAPIII. The effect of M protein alone on transcription by RNAPI-, RNAPII-, and RNAPIII-dependent promoters was measured by cotransfection assays. M protein inhibited transcription from RNAPI- and RNAPII-dependent promoters in the absence of other viral gene products. RNAPIII-dependent transcription of the adenovirus VA promoters was also inhibited by M protein. However, as observed during wt VSV infection, M protein enhanced endogenous 5S rRNA transcription, indicating that the inhibition of transcription by RNAPIII was dependent on the nature of the promoter.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC 27157. Phone: (336) 716-4237. Fax: (336) 716-9928. E-mail: dlyles{at}wfubmc.edu.

Journal of Virology, October 1998, p. 8413-8419, Vol. 72, No. 10
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Ghildyal, R., Ho, A., Dias, M., Soegiyono, L., Bardin, P. G., Tran, K. C., Teng, M. N., Jans, D. A. (2009). The Respiratory Syncytial Virus Matrix Protein Possesses a Crm1-Mediated Nuclear Export Mechanism. J. Virol. 83: 5353-5362 [Abstract] [Full Text]  
  • Boonyaratanakornkit, J. B., Bartlett, E. J., Amaro-Carambot, E., Collins, P. L., Murphy, B. R., Schmidt, A. C. (2009). The C Proteins of Human Parainfluenza Virus Type 1 (HPIV1) Control the Transcription of a Broad Array of Cellular Genes That Would Otherwise Respond to HPIV1 Infection. J. Virol. 83: 1892-1910 [Abstract] [Full Text]  
  • Pettit Kneller, E. L., Connor, J. H., Lyles, D. S. (2009). hnRNPs Relocalize to the Cytoplasm following Infection with Vesicular Stomatitis Virus. J. Virol. 83: 770-780 [Abstract] [Full Text]  
  • Renukaradhya, G. J., Khan, M. A., Shaji, D., Brutkiewicz, R. R. (2008). Vesicular Stomatitis Virus Matrix Protein Impairs CD1d-Mediated Antigen Presentation through Activation of the p38 MAPK Pathway. J. Virol. 82: 12535-12542 [Abstract] [Full Text]  
  • Carey, B. L., Ahmed, M., Puckett, S., Lyles, D. S. (2008). Early Steps of the Virus Replication Cycle Are Inhibited in Prostate Cancer Cells Resistant to Oncolytic Vesicular Stomatitis Virus. J. Virol. 82: 12104-12115 [Abstract] [Full Text]  
  • Zhao, J.-m., Wen, Y.-j., Li, Q., Wang, Y.-s., Wu, H.-b., Xu, J.-r., Chen, X.-c., Wu, Y., Fan, L.-y., Yang, H.-s., Liu, T., Ding, Z.-y., Du, X.-b., Diao, P., Li, J., Wu, H.-b., Kan, B., Lei, S., Deng, H.-x., Mao, Y.-q., Zhao, X., Wei, Y.-q. (2008). A promising cancer gene therapy agent based on the matrix protein of vesicular stomatitis virus. FASEB J. 22: 4272-4280 [Abstract] [Full Text]  
  • Vogt, C., Preuss, E., Mayer, D., Weber, F., Schwemmle, M., Kochs, G. (2008). The Interferon Antagonist ML Protein of Thogoto Virus Targets General Transcription Factor IIB. J. Virol. 82: 11446-11453 [Abstract] [Full Text]  
  • Mayuri, , Geders, T. W., Smith, J. L., Kuhn, R. J. (2008). Role for Conserved Residues of Sindbis Virus Nonstructural Protein 2 Methyltransferase-Like Domain in Regulation of Minus-Strand Synthesis and Development of Cytopathic Infection. J. Virol. 82: 7284-7297 [Abstract] [Full Text]  
  • Whitlow, Z. W., Connor, J. H., Lyles, D. S. (2008). New mRNAs Are Preferentially Translated during Vesicular Stomatitis Virus Infection. J. Virol. 82: 2286-2294 [Abstract] [Full Text]  
  • Randall, R. E., Goodbourn, S. (2008). Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. J. Gen. Virol. 89: 1-47 [Abstract] [Full Text]  
  • Ciancanelli, M. J., Basler, C. F. (2006). Mutation of YMYL in the Nipah Virus Matrix Protein Abrogates Budding and Alters Subcellular Localization. J. Virol. 80: 12070-12078 [Abstract] [Full Text]  
  • Reuter, T., Weissbrich, B., Schneider-Schaulies, S., Schneider-Schaulies, J. (2006). RNA Interference with Measles Virus N, P, and L mRNAs Efficiently Prevents and with Matrix Protein mRNA Enhances Viral Transcription.. J. Virol. 80: 5951-5957 [Abstract] [Full Text]  
  • Gaddy, D. F., Lyles, D. S. (2005). Vesicular Stomatitis Viruses Expressing Wild-Type or Mutant M Proteins Activate Apoptosis through Distinct Pathways. J. Virol. 79: 4170-4179 [Abstract] [Full Text]  
  • Kopecky, S. A., Lyles, D. S. (2003). The Cell-Rounding Activity of the Vesicular Stomatitis Virus Matrix Protein Is due to the Induction of Cell Death. J. Virol. 77: 5524-5528 [Abstract] [Full Text]  
  • Ahmed, M., McKenzie, M. O., Puckett, S., Hojnacki, M., Poliquin, L., Lyles, D. S. (2003). Ability of the Matrix Protein of Vesicular Stomatitis Virus To Suppress Beta Interferon Gene Expression Is Genetically Correlated with the Inhibition of Host RNA and Protein Synthesis. J. Virol. 77: 4646-4657 [Abstract] [Full Text]  
  • Kopecky, S. A., Lyles, D. S. (2003). Contrasting Effects of Matrix Protein on Apoptosis in HeLa and BHK Cells Infected with Vesicular Stomatitis Virus Are due to Inhibition of Host Gene Expression. J. Virol. 77: 4658-4669 [Abstract] [Full Text]  
  • Frolova, E. I., Fayzulin, R. Z., Cook, S. H., Griffin, D. E., Rice, C. M., Frolov, I. (2002). Roles of Nonstructural Protein nsP2 and Alpha/Beta Interferons in Determining the Outcome of Sindbis Virus Infection. J. Virol. 76: 11254-11264 [Abstract] [Full Text]  
  • Kopecky, S. A., Willingham, M. C., Lyles, D. S. (2001). Matrix Protein and Another Viral Component Contribute to Induction of Apoptosis in Cells Infected with Vesicular Stomatitis Virus. J. Virol. 75: 12169-12181 [Abstract] [Full Text]  
  • Harty, R. N., Brown, M. E., McGettigan, J. P., Wang, G., Jayakar, H. R., Huibregtse, J. M., Whitt, M. A., Schnell, M. J. (2001). Rhabdoviruses and the Cellular Ubiquitin-Proteasome System: a Budding Interaction. J. Virol. 75: 10623-10629 [Abstract] [Full Text]  
  • Terstegen, L., Gatsios, P., Ludwig, S., Pleschka, S., Jahnen-Dechent, W., Heinrich, P. C., Graeve, L. (2001). The Vesicular Stomatitis Virus Matrix Protein Inhibits Glycoprotein 130-Dependent STAT Activation. J. Immunol. 167: 5209-5216 [Abstract] [Full Text]  
  • Yuan, H., Puckett, S., Lyles, D. S. (2001). Inhibition of Host Transcription by Vesicular Stomatitis Virus Involves a Novel Mechanism That Is Independent of Phosphorylation of TATA-Binding Protein (TBP) or Association of TBP with TBP-Associated Factor Subunits. J. Virol. 75: 4453-4458 [Abstract] [Full Text]  
  • Lyles, D. S. (2000). Cytopathogenesis and Inhibition of Host Gene Expression by RNA Viruses. Microbiol. Mol. Biol. Rev. 64: 709-724 [Abstract] [Full Text]  
  • Petersen, J. M., Her, L.-S., Varvel, V., Lund, E., Dahlberg, J. E. (2000). The Matrix Protein of Vesicular Stomatitis Virus Inhibits Nucleocytoplasmic Transport When It Is in the Nucleus and Associated with Nuclear Pore Complexes. Mol. Cell. Biol. 20: 8590-8601 [Abstract] [Full Text]  
  • Chiou, P. P., Kim, C. H., Ormonde, P., Leong, J.-A. C. (2000). Infectious Hematopoietic Necrosis Virus Matrix Protein Inhibits Host-Directed Gene Expression and Induces Morphological Changes of Apoptosis in Cell Cultures. J. Virol. 74: 7619-7627 [Abstract] [Full Text]  
  • Ball, L. A., Pringle, C. R., Flanagan, B., Perepelitsa, V. P., Wertz, G. W. (1999). Phenotypic Consequences of Rearranging the P, M, and G Genes of Vesicular Stomatitis Virus. J. Virol. 73: 4705-4712 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»