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Internal ribosome entry sequence‐mediated translation initiation triggers nonsense‐mediated decay
Author(s) -
Holbrook Jill A,
NeuYilik Gabriele,
Gehring Niels H,
Kulozik Andreas E,
Hentze Matthias W
Publication year - 2006
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400721
Subject(s) - nonsense mediated decay , eukaryotic translation , translation (biology) , internal ribosome entry site , sequence (biology) , initiation factor , protein biosynthesis , ribosome , biology , microbiology and biotechnology , eif4e , computational biology , genetics , chemistry , rna , messenger rna , gene , rna splicing
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.