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Related Experiment Videos

A novel functional human eukaryotic translation initiation factor 4G

A Gradi1, H Imataka, Y V Svitkin

  • 1Department of Biochemistry and McGill Cancer Center, McGill University, Montréal, Québec, Canada.

Molecular and Cellular Biology
|January 7, 1998
PubMed
Summary

Researchers discovered a new protein, eIF4GII, which is a functional homolog of eIF4GI. This finding is crucial for understanding how viruses shut down host protein synthesis during infection.

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Area of Science:

  • Molecular Biology
  • Virology
  • Biochemistry

Background:

  • The eukaryotic translation initiation factor 4F (eIF4F) complex is vital for protein synthesis.
  • Mammals possess one known eIF4G subunit (eIF4GI), unlike yeast and plants which have two.
  • The function of a potential second mammalian eIF4G homolog remained uncharacterized.

Purpose of the Study:

  • To discover and functionally characterize a novel mammalian eIF4G homolog, designated eIF4GII.
  • To determine the interaction partners and functional relevance of eIF4GII in protein synthesis and viral infection.

Main Methods:

  • Sequence homology analysis to identify eIF4GII.
  • Far-Western analysis and coimmunoprecipitation to assess protein interactions.
  • Cap affinity chromatography to confirm complex formation.

Related Experiment Videos

  • Functional assays using reticulocyte lysates to evaluate translation restoration.

    • Main Results:

    • A novel eIF4G homolog, eIF4GII, was identified with 46% amino acid identity to eIF4GI.
    • eIF4GII directly interacts with key translation factors eIF4E, eIF4A, and eIF3.
    • eIF4GII is cleaved by picornaviruses and can restore cap-dependent translation inhibited by viral proteases.
    • eIF4GII forms a complex with eIF4E in HeLa cells.

    Conclusions:

    • eIF4GII is a functional homolog of eIF4GI in mammals.
    • eIF4GII plays a role in cap-dependent translation and is targeted by picornaviruses.
    • The discovery of eIF4GII provides new insights into viral strategies for host protein synthesis shutoff.