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EMBO reports 9, 5, 446–451 (2008)
doi:10.1038/embor.2008.36
AOP Published online: 28 March 2008
NMD resulting from encephalomyocarditis virus IRES-directed translation initiation seems to be restricted to CBP80/20-bound mRNA
Collynn F Woeller, Martina Gaspari†, Olaf Isken & Lynne E Maquat
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Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box 712, Rochester, New York 14642, USA
To whom correspondence should be addressed
Lynne E Maquat Tel: +1 585 273 5640; Fax: +1 585 271 2683; E-mail: lynne_maquat@urmc.rochester.edu
† Present address: Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA
Received 11 December 2007; Accepted 14 February 2008; Published online 28 March 2008.
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Abstract
Nonsense-mediated messenger RNA decay (NMD) generally degrades mRNAs that prematurely terminate translation as a means of quality control. NMD in mammalian cells targets newly spliced mRNA that is bound by the cap-binding protein heterodimer CBP80/20 and one or more post-splicing exon junction complexes during a pioneer round of translation. NMD targets mRNA that initiates translation using the encephalomyocarditis virus (EMCV) internal ribosome entry site (IRES), therefore NMD might target not only CBP80/20-bound mRNA but also its remodelled product, eIF4E-bound mRNA. Here, we provide evidence that NMD triggered by translation initiation at the EMCV IRES, similar to NMD triggered by translation initiation at an mRNA cap, targets CBP80/20-bound mRNA but does not detectably target eIF4E-bound mRNA. We show that EMCV IRES-initiated translation undergoes a CBP80/20-associated pioneer round of translation that results in CBP80/20-dependent and Upf factor-dependent NMD when translation terminates prematurely.
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