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Nucleic Acids Research Advance Access originally published online on August 13, 2007
Nucleic Acids Research 2007 35(16):5409-5421; doi:10.1093/nar/gkm524
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Nucleic Acids Research, 2007, Vol. 35, No. 16 5409-5421
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

RNA

Translational control of the interferon regulatory factor 2 mRNA by IRES element

Debojyoti Dhar, Swagata Roy and Saumitra Das*

Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore-560012, India

*To whom correspondence should be addressed. Tel: +91 80 293 2886; Fax: +91 80 360 2697; Email: sdas{at}mcbl.iisc.ernet.in

Received May 17, 2007. Revised June 22, 2007. Accepted June 22, 2007.

Translational control represents an important mode of regulation of gene expression under stress conditions. We have studied the translation of interferon regulatory factor 2 (IRF2) mRNA, a negative regulator of transcription of interferon-stimulated genes and demonstrated the presence of internal ribosome entry site (IRES) element in the 5'UTR of IRF2 RNA. Various control experiments ruled out the contribution of leaky scanning, cryptic promoter activity or RNA splicing in the internal initiation of IRF2 RNA. It seems IRF2-IRES function is not sensitive to eIF4G cleavage, since its activity was only marginally affected in presence of Coxsackievirus 2A protease. Interferon {alpha} treatment did not affect the IRF2-IRES activity or the protein level significantly. Also, in cells treated with tunicamycin [an agent causing endoplasmic reticulum (ER) stress], the IRF2-IRES activity and the protein levels were unaffected, although the cap-dependent translation was severely impaired. Analysis of the cellular protein binding with the IRF2-IRES suggests certain cellular factors, which might influence its function under stress conditions. Interestingly, partial knockdown of PTB protein significantly inhibited the IRF2-IRES function. Taken together, it appears that IRF2 gene expression during stress condition is controlled by the IRES element, which in turn influences the cellular response.


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