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Updated: Jun 17, 2026
09:26
Identification of Footprints of RNA:Protein Complexes via RNA Immunoprecipitation in Tandem Followed by Sequencing (RIPiT-Seq)
Published on: July 10, 2019
Nonsense-mediated translational repression involves exon junction complex downstream of premature translation
Hyung Chul Lee1, Nara Oh, Hana Cho
1School of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
FEBS Letters
|January 14, 2010
Summary
Human TGFbetaR2 mRNA with premature stop codons undergoes translational repression, not decay. Exon junction complexes inhibit translation after 80S ribosome formation, acting as negative regulators.
Area of Science:
- Molecular Biology
- RNA Biology
- Gene Regulation
Background:
- Nonsense-mediated mRNA decay (NMD) and translational repression (NMTR) eliminate aberrant mRNAs.
- Transforming growth factor-beta receptor type 2 (TGFbetaR2) mRNA with premature translation termination codons (PTCs) are primarily subject to NMTR.
Purpose of the Study:
- To investigate the role of exon junction complex (EJC) in the NMTR of TGFbetaR2 mRNA.
- To elucidate the mechanism by which EJCs regulate translation downstream of a PTC.
Main Methods:
- Utilized internal ribosome entry sites (IRESes) to study translation.
- Investigated the impact of core EJC components on TGFbetaR2 mRNA translation.
- Analyzed ribosome complex formation.
Main Results:
- EJCs downstream of a PTC inhibit the translation of TGFbetaR2 mRNA.
- Translational repression mediated by core EJC components occurs post-80S ribosome complex formation.
- Different IRES elements confirmed the inhibitory role of EJCs.
Conclusions:
- Exon junction complexes function as negative regulators of translation for specific mRNAs.
- Core EJC components play a critical role in the NMTR pathway.
- Findings provide new insights into post-transcriptional gene regulation mechanisms.
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