Nonsense-mediated translational repression involves exon junction complex downstream of premature translation termination codon

Hyung Chul Lee, Nara Oh, Hana Cho, Junho Choe, Yoon Ki Kim

    Research output: Contribution to journalArticlepeer-review

    15 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)795-800
    Number of pages6
    JournalFEBS Letters
    Volume584
    Issue number4
    DOIs
    Publication statusPublished - 2010 Feb

    Bibliographical note

    Funding Information:
    We thank Lynne E. Maquat for providing NMD reporter plasmids, pCMV-myc-Upf1 WT, and α-Upfs antibodies, Robin Reed for α-eIF4AIII antibody, Gideon Dreyfuss for α-Y14, Hoguen Kim for the TGFβR2 gene, and Sung Key Jang and Peter Sarnow for IRES-containing plasmids. This study was supported by a grant of the Korea Healthcare technology R&D Project, Ministry for Health, Welfare & Family Affairs, Republic of Korea ( A090027 ).

    Keywords

    • EIF4AIII
    • EJC
    • NMD
    • NMTR
    • Y14

    ASJC Scopus subject areas

    • Biophysics
    • Structural Biology
    • Biochemistry
    • Molecular Biology
    • Genetics
    • Cell Biology

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