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EMBO reports 7, 7, 722–726 (2006)
doi:10.1038/sj.embor.7400721
AOP Published online: 16 June 2006
Internal ribosome entry sequence-mediated translation initiation triggers nonsense-mediated decay
Jill A Holbrook1, 2, Gabriele Neu-Yilik1, 2, Niels H Gehring1, 2, Andreas E Kulozik1, 2 & Matthias W Hentze1, 3
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1 Molecular Medicine Partnership Unit, University of Heidelberg and European Molecular Biology Laboratory, University Hospital Heidelberg, Im Neuenheimer Feld 150, Heidelberg 69120, Germany
2 Department for Pediatric Oncology, Hematology and Immunology, University Hospital Heidelberg, Im Neuenheimer Feld 150, Heidelberg 69120, Germany
3 Gene Expression Unit, European Molecular Biology Laboratory, Meyerhofstrasse 1, Heidelberg 69117, Germany
To whom correspondence should be addressed
Andreas E Kulozik Tel: +49 6221 56 2303; Fax: +49 6221 56 4559; E-mail: andreas.kulozik@med.uni-heidelberg.de
Matthias W Hentze Tel: +49 6221 387 501; Fax: +49 6221 387 518; E-mail: hentze@embl.de
Received 2 March 2006; Accepted 10 May 2006; Published online 16 June 2006.
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Abstract
In eukaryotes, a surveillance pathway known as nonsense-mediated decay (NMD) regulates the abundance of messenger RNAs containing premature termination codons (PTCs). In mammalian cells, it has been asserted that the NMD-relevant first round of translation is special and involves initiation by a specific protein heterodimer, the nuclear cap-binding complex (CBC). Arguing against a requirement for CBC-mediated translation initiation, we show that ribosomal recruitment by the internal ribosomal entry sequence of the encephalomyocarditis virus triggers NMD of a PTC-containing transcript under conditions in which ribosome entry from the cap is prohibited. These data generalize the previous model and suggest that translation per se, irrespective of how it is initiated, can mediate NMD.
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