This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental material
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
Google Scholar
Right arrow Articles by Cairrao, F.
Right arrow Articles by Vanzo, N.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cairrao, F.
Right arrow Articles by Vanzo, N.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, May 2009, p. 2636-2643, Vol. 29, No. 10
0270-7306/09/$08.00+0     doi:10.1128/MCB.01506-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

AU-Rich Elements Regulate Drosophila Gene Expression{triangledown} ,{dagger}

Fatima Cairrao,1 Anason S. Halees,2 Khalid S. A. Khabar,2 Dominique Morello,1 and Nathalie Vanzo1*

CBD, UMR 5547, CNRS-UPS, 31062 Toulouse Cedex 4, France,1 Biomolecular Research Program, King Faisal Specialist Hospital and Research Center, Riyadh 11211, Saudi Arabia2

Received 26 September 2008/ Returned for modification 11 November 2008/ Accepted 23 February 2009

In mammals, AU-rich elements (AREs) are critical regulators of mRNA turnover. They recruit ARE-binding proteins that inhibit or stimulate rapid mRNA degradation in response to stress or developmental cues. Using a bioinformatics approach, we have identified AREs in Drosophila melanogaster 3' untranslated regions and validated their cross-species conservation in distant Drosophila genomes. We have generated a Drosophila ARE database (D-ARED) and established that about 16% of D. melanogaster genes contain the mammalian ARE signature, an AUUUA pentamer in an A/U-rich context. Using candidate ARE genes, we show that Drosophila AREs stimulate reporter mRNA decay in cultured cells and in the physiological context of the immune response in D. melanogaster. In addition, we found that the conserved ARE-binding protein Tis11 regulates temporal gene expression through ARE-mediated decay (AMD) in D. melanogaster. Our work reveals that AREs are conserved and functional cis regulators of mRNA decay in Drosophila and highlights this organism as a novel model system to unravel in vivo the contribution of AMD to various processes.

* Corresponding author. Mailing address: Centre de Biologie du développement, UMR 5547, CNRS-Université Paul Sabatier, 31062 Toulouse Cedex 4, France. Phone: 33 05 61 55 65 08. Fax: 33 05 61 55 65 07. E-mail: vanzo{at}cict.fr

{triangledown} Published ahead of print on 9 March 2009.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, May 2009, p. 2636-2643, Vol. 29, No. 10
0270-7306/09/$08.00+0     doi:10.1128/MCB.01506-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hong, X., Hammell, M., Ambros, V., Cohen, S. M. (2009). Immunopurification of Ago1 miRNPs selects for a distinct class of microRNA targets. Proc. Natl. Acad. Sci. USA 106: 15085-15090 [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»