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Nucleic Acids Research Advance Access originally published online on April 9, 2009
Nucleic Acids Research 2009 37(11):3612-3624; doi:10.1093/nar/gkp223
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Nucleic Acids Research, 2009, Vol. 37, No. 11 3612-3624
© 2009 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

Alternative polyadenylation variants of the RNA binding protein, HuR: abundance, role of AU-rich elements and auto-Regulation

Wijdan Al-Ahmadi, Maha Al-Ghamdi, Latifa Al-Haj, Maher Al-Saif and Khalid S. A. Khabar*

Program in Biomolecular Research, King Faisal Specialist Hospital and Research Center, Riyadh 11211, Saudi Arabia

*To whom correspondence should be addressed. Tel: +966 1 442 7876; Fax: +966 1 442 4182; Email: khabar{at}kfshrc.edu.sa

Received August 6, 2008. Revised March 21, 2009. Accepted March 23, 2009.

The RNA-binding protein, HuR, is involved in the stabilization of AU-rich element-containing mRNAs with products that are involved in cell-cycle progression, cell differentiation and inflammation. We show that there are multiple polyadenylation variants of HuR mRNA that differ in their abundance, using both bioinformatics and experimental approaches. A polyadenylation variant with distal poly(A) signal is a rare transcript that harbors functional AU-rich elements (ARE) in the 3'UTR. A minimal 60-nt region, but not a mutant form, fused to reporter-3'UTR constructs was able to downregulate the reporter activity. The most predominant and alternatively polyadenylated mature transcript does not contain the ARE. HuR itself binds HuR mRNA, and upregulated the activity of reporter from constructs fused with ARE-isoform and the HuR ARE. Wild-type tristetraprolin (TTP), but not the zinc finger mutant TTP, competes for HuR binding and upregulation of HuR mRNA. The study shows that the HuR gene codes for several polyadenylation variants differentially regulated by AU-rich elements, and demonstrates an auto-regulatory role of HuR.

The authors wish it to be known that, in their opinion, the second and third authors should be regarded as joint First Authors.


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