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Open Access Highly Accessed Research

RNA-editing-mediated exon evolution

Galit Lev-Maor1, Rotem Sorek12, Erez Y Levanon34, Nurit Paz5, Eli Eisenberg6 and Gil Ast1*

Author Affiliations

1 Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel

2 Genomics Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA

3 Compugen Ltd, Pinchas Rosen St, Tel-Aviv 69512, Israel

4 Department of Genetics, Harvard Medical School, Avenue Louis Pasteur, Boston, Massachusetts 02115, USA

5 Department of Pediatric Hemato-Oncology, Chaim Sheba Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel

6 School of Physics and Astronomy, Raymond and Beverly Sackler Faculty of Exact Sciences, Tel-Aviv University, Ramat Aviv 69978, Israel

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Genome Biology 2007, 8:R29  doi:10.1186/gb-2007-8-2-r29

Published: 27 February 2007

Abstract

Background

Alu retroelements are specific to primates and abundant in the human genome. Through mutations that create functional splice sites within intronic Alus, these elements can become new exons in a process denoted exonization. It was recently shown that Alu elements are also heavily changed by RNA editing in the human genome.

Results

Here we show that the human nuclear prelamin A recognition factor contains a primate-specific Alu-exon that exclusively depends on RNA editing for its exonization. We demonstrate that RNA editing regulates the exonization in a tissue-dependent manner, through both the creation of a functional AG 3' splice site, and alteration of functional exonic splicing enhancers within the exon. Furthermore, a premature stop codon within the Alu-exon is eliminated by an exceptionally efficient RNA editing event. The sequence surrounding this editing site is important not only for editing of that site but also for editing in other neighboring sites as well.

Conclusion

Our results show that the abundant RNA editing of Alu sequences can be recruited as a mechanism supporting the birth of new exons in the human genome.