Translational repression of NMD targets by GIGYF2 and EIF4E2

Boris Zinshteyn, Niladri K. Sinha, Syed Usman Enam, Benjamin Koleske, Rachel Green

Research output: Contribution to journalArticlepeer-review

Abstract

Translation of messenger RNAs (mRNAs) with premature termination codons produces truncated proteins with potentially deleterious effects. This is prevented by nonsense-mediated mRNA decay (NMD) of these mRNAs. NMD is triggered by ribosomes terminating upstream of a splice site marked by an exon-junction complex (EJC), but also acts on many mRNAs lacking a splice junction after their termination codon. We developed a genome-wide CRISPR flow cytometry screen to identify regulators of mRNAs with premature termination codons in K562 cells. This screen recovered essentially all core NMD factors and suggested a role for EJC factors in degradation of PTCs without downstream splicing. Among the strongest hits were the translational repressors GIGYF2 and EIF4E2. GIGYF2 and EIF4E2 mediate translational repression but not mRNA decay of a subset of NMD targets and interact with NMD factors genetically and physically. Our results suggest a model wherein recognition of a stop codon as premature can lead to its translational repression through GIGYF2 and EIF4E2.

Original languageEnglish (US)
Article numbere1009813
JournalPLoS genetics
Volume17
Issue number10 October
DOIs
StatePublished - Oct 19 2021

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Molecular Biology
  • Genetics
  • Genetics(clinical)
  • Cancer Research

Fingerprint

Dive into the research topics of 'Translational repression of NMD targets by GIGYF2 and EIF4E2'. Together they form a unique fingerprint.

Cite this