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

doi:10.1016/j.febslet.2010.01.003

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

Department of Life Sciences

Research output: Contribution to journal › Article › peer-review

13 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 language	English
Pages (from-to)	795-800
Number of pages	6
Journal	FEBS Letters
Volume	584
Issue number	4
DOIs	https://doi.org/10.1016/j.febslet.2010.01.003
Publication status	Published - 2010 Feb

Keywords

EIF4AIII
EJC
NMD
NMTR
Y14

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2010.01.003

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@article{3da4f62e3fd44603ac07d12b743478c0,

title = "Nonsense-mediated translational repression involves exon junction complex downstream of premature translation termination codon",

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.",

keywords = "EIF4AIII, EJC, NMD, NMTR, Y14",

author = "Lee, {Hyung Chul} and Nara Oh and Hana Cho and Junho Choe and Kim, {Yoon Ki}",

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 ). ",

year = "2010",

month = feb,

doi = "10.1016/j.febslet.2010.01.003",

language = "English",

volume = "584",

pages = "795--800",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

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TY - JOUR

T1 - Nonsense-mediated translational repression involves exon junction complex downstream of premature translation termination codon

AU - Lee, Hyung Chul

AU - Oh, Nara

AU - Cho, Hana

AU - Choe, Junho

AU - Kim, Yoon Ki

N1 - 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 ).

PY - 2010/2

Y1 - 2010/2

N2 - 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.

AB - 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.

KW - EIF4AIII

KW - EJC

KW - NMD

KW - NMTR

KW - Y14

UR - http://www.scopus.com/inward/record.url?scp=77649274260&partnerID=8YFLogxK

U2 - 10.1016/j.febslet.2010.01.003

DO - 10.1016/j.febslet.2010.01.003

M3 - Article

C2 - 20067791

AN - SCOPUS:77649274260

SN - 0014-5793

VL - 584

SP - 795

EP - 800

JO - FEBS Letters

JF - FEBS Letters

IS - 4

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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