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 Pampin, M.
Right arrow Articles by Chelbi-Alix, M. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pampin, M.
Right arrow Articles by Chelbi-Alix, M. K.

 Previous Article  |  Next Article 

Journal of Virology, September 2006, p. 8582-8592, Vol. 80, No. 17
0022-538X/06/$08.00+0     doi:10.1128/JVI.00031-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Cross Talk between PML and p53 during Poliovirus Infection: Implications for Antiviral Defense

Mathieu Pampin,1 Yannick Simonin,2 Bruno Blondel,2 Yann Percherancier,1 and Mounira K. Chelbi-Alix1*

CNRS FRE 2944, Institut Lwoff, 7 rue Guy Moquet, 94801 Villejuif, France,1 Institut Pasteur, 75724 Paris, France2

Received 4 January 2006/ Accepted 12 June 2006

PML nuclear bodies (NBs) are dynamic intranuclear structures harboring numerous transiently or permanently localized proteins. PML, the NBs' organizer, is directly induced by interferon, and its expression is critical for antiviral host defense. We describe herein the molecular events following poliovirus infection that lead to PML-dependent p53 activation and protection against virus infection. Poliovirus infection induces PML phosphorylation through the extracellular signal-regulated kinase pathway, increases PML SUMOylation, and induces its transfer from the nucleoplasm to the nuclear matrix. These events result in the recruitment of p53 to PML NBs, p53 phosphorylation on Ser15, and activation of p53 target genes leading to the induction of apoptosis. Moreover, the knock-down of p53 by small interfering RNA results in higher poliovirus replication, suggesting that p53 participates in antiviral defense. This effect, which requires the presence of PML, is transient since poliovirus targets p53 by inducing its degradation in a proteasome- and MDM2-dependent manner. Our results provide evidence of how poliovirus counteracts p53 antiviral activity by regulating PML and NBs, thus leading to p53 degradation.


* Corresponding author. Mailing address: CNRS FRE 2944, Institut Lwoff, 7 rue Guy Moquet, Villejuif 94801, France. Phone: 33 1 49 58 33 51. Fax: 33 1 49 58 33 48. E-mail: mchelbi{at}vjf.cnrs.fr.


Journal of Virology, September 2006, p. 8582-8592, Vol. 80, No. 17
0022-538X/06/$08.00+0     doi:10.1128/JVI.00031-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Lidsky, P. V., Romanova, L. I., Kolesnikova, M. S., Bardina, M. V., Khitrina, E. V., Hato, S. V., van Kuppeveld, F. J. M., Agol, V. I. (2009). Interactions between Viral and Prokaryotic Pathogens in a Mixed Infection with Cardiovirus and Mycoplasma. J. Virol. 83: 9940-9951 [Abstract] [Full Text]  
  • Munoz-Fontela, C., Macip, S., Martinez-Sobrido, L., Brown, L., Ashour, J., Garcia-Sastre, A., Lee, S. W., Aaronson, S. A. (2008). Transcriptional role of p53 in interferon-mediated antiviral immunity. JEM 205: 1929-1938 [Abstract] [Full Text]  
  • Chang, S.-S., Lo, Y.-C., Chua, H.-H., Chiu, H.-Y., Tsai, S.-C., Chen, J.-Y., Lo, K.-W., Tsai, C.-H. (2008). Critical Role of p53 in Histone Deacetylase Inhibitor-Induced Epstein-Barr Virus Zta Expression. J. Virol. 82: 7745-7751 [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]  
  • Kofod-Olsen, E., Ross-Hansen, K., Mikkelsen, J. G., Hollsberg, P. (2008). Human herpesvirus 6B U19 protein is a PML-regulated transcriptional activator that localizes to nuclear foci in a PML-independent manner. J. Gen. Virol. 89: 106-116 [Abstract] [Full Text]  
  • Baltzis, D., Pluquet, O., Papadakis, A. I., Kazemi, S., Qu, L.-K., Koromilas, A. E. (2007). The eIF2{alpha} Kinases PERK and PKR Activate Glycogen Synthase Kinase 3 to Promote the Proteasomal Degradation of p53. J. Biol. Chem. 282: 31675-31687 [Abstract] [Full Text]  
  • Groskreutz, D. J., Monick, M. M., Yarovinsky, T. O., Powers, L. S., Quelle, D. E., Varga, S. M., Look, D. C., Hunninghake, G. W. (2007). Respiratory Syncytial Virus Decreases p53 Protein to Prolong Survival of Airway Epithelial Cells. J. Immunol. 179: 2741-2747 [Abstract] [Full Text]