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Nonsense‐mediated translational repression involves exon junction complex downstream of premature translation termination codon
Author(s) -
Lee Hyung Chul,
Oh Nara,
Cho Hana,
Choe Junho,
Kim Yoon Ki
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.01.003
Subject(s) - frameshift mutation , translation (biology) , nonsense mutation , psychological repression , microbiology and biotechnology , start codon , exon , nonsense mediated decay , five prime untranslated region , eukaryotic translation , messenger rna , translational regulation , biology , stop codon , genetics , chemistry , mutation , rna splicing , gene , rna , gene expression , missense mutation
Human transforming growth factor‐β receptor type 2 (TGFβR2) mRNA harboring a premature translation termination codon (PTC) generated by frameshift mutation is targeted for nonsense‐mediated translational repression (NMTR), rather than nonsense‐mediated mRNA decay (NMD). Here we show that exon junction complex (EJC) downstream of a PTC plays an inhibitory role in translation of TGFβR2 mRNA. Translational repression by core EJC components occurs after formation of 80S ribosome complex, which is demonstrated using different types of internal ribosome entry sites (IRESes). Our findings implicate EJCs or core EJC components as negative regulators of translation.