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 Mesplède, T.
Right arrow Articles by Navarro, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mesplède, T.
Right arrow Articles by Navarro, S.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, October 2005, p. 8717-8731, Vol. 25, No. 19
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.19.8717-8731.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

The POU Transcription Factor Oct-1 Represses Virus-Induced Interferon A Gene Expression

Thibault Mesplède,1 Marie-Laure Island,1 Nicolas Christeff,1 Fahrettin Petek,2 Janine Doly,2 and Sébastien Navarro1*

Laboratoire de Régulation de la Transcription et Maladies Génétiques, CNRS, UPR 2228,1 Laboratoire de Régulation de la Transcription des Gènes Eucaryotes, UPR 37, UFR Biomédicale des Saints-Pères, Université René Descartes, 45 Rue des Saints-Pères, 75270 Paris Cedex 06, France2

Received 21 January 2005/ Returned for modification 5 April 2005/ Accepted 11 July 2005

Alpha interferon (IFN-{alpha}) and IFN-ß are able to interfere with viral infection. They exert a vast array of biologic functions, including growth arrest, cell differentiation, and immune system regulation. This regulation extends from innate immunity to cellular and humoral adaptive immune responses. A strict control of expression is needed to prevent detrimental effects of unregulated IFN. Multiple IFN-A subtypes are coordinately induced in human and mouse cells infected by virus and exhibit differences in expression of their individual mRNAs. We demonstrated that the weakly expressed IFN-A11 gene is negatively regulated after viral infection, due to a distal negative regulatory element, binding homeoprotein pituitary homeobox 1 (Pitx1). Here we show that the POU protein Oct-1 binds in vitro and in vivo to the IFN-A11 promoter and represses IFN-A expression upon interferon regulatory factor overexpression. Furthermore, we show that Oct-1-deficient MEFs exhibit increased in vivo IFN-A gene expression and increased antiviral activity. Finally, the IFN-A expression pattern is modified in Oct-1-deficient MEFs. The broad representation of effective and potent octamer-like sequences within IFN-A promoters suggests an important role for Oct-1 in IFN-A regulation.


* Corresponding author. Mailing address: Laboratoire de Régulation de la Transcription et Maladies Génétiques, CNRS, UPR 2228, UFR Biomédicale des Saints-Pères, Université René Descartes, 45 Rue des Saints-Pères, 75270 Paris Cedex 06, France. Phone: 33-1-42-86-22-74. Fax: 33-1-42-86-20-42. E-mail: sebastien.navarro{at}univ-paris5.fr.


Molecular and Cellular Biology, October 2005, p. 8717-8731, Vol. 25, No. 19
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.19.8717-8731.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Wu, C., Hu, Z., Yu, D., Huang, L., Jin, G., Liang, J., Guo, H., Tan, W., Zhang, M., Qian, J., Lu, D., Wu, T., Lin, D., Shen, H. (2009). Genetic Variants on Chromosome 15q25 Associated with Lung Cancer Risk in Chinese Populations. Cancer Res. 69: 5065-5072 [Abstract] [Full Text]