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4EHP and GIGYF1/2 Mediate Translation-Coupled Messenger RNA Decay

  1. Author:
    Weber, Ramona
    Chung, Min-Yi
    Keskeny, Csilla
    Zinnall, Ulrike
    Landthaler, Markus
    Valkov,Eugene
    Izaurralde, Elisa
    Igreja, Catie

  2. Author Address

    Max Planck Inst Dev Biol, Dept Biochem, Max Planck Ring 5, D-72076 Tubingen, Germany.Max Delbruck Ctr Mol Med Helmholtz Assoc MDC, Berlin Inst Med Syst Biol BIMSB, D-10115 Berlin, Germany.Humboldt Univ, Inst Biol, IRI Life Sci, D-10115 Berlin, Germany.Max Delbruck Ctr, Expt & Clin Res Ctr ECRC, D-13125 Berlin, Germany.Charite, D-13125 Berlin, Germany.NCI, Messenger RNA Regulat & Decay Sect, RNA Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA.
    1. Year: 2020
    2. Date: OCT 13
  2. Journal: CELL REPORTS
  3. CELL PRESS,
    1. 33
    2. 2
  5. Type of Article: Article
  6. Article Number: 108262
  7. ISSN: 2211-1247
  1. Abstract:

    Current models of mRNA turnover indicate that cytoplasmic degradation is coupled with translation. However, our understanding of the molecular events that coordinate ribosome transit with the mRNA decay machinery is still limited. Here, we show that 4EHP-GIGYF1/2 complexes trigger co-translational mRNA decay. Human cells lacking these proteins accumulate mRNAs with prominent ribosome pausing. They include, among others, transcripts encoding secretory and membrane-bound proteins or tubulin subunits. In addition, 4EHP-GIGYF1/2 complexes fail to reduce mRNA levels in the absence of ribosome stalling or upon disruption of their interaction with the cap structure, DDX6, and ZNF598. We further find that co-translational binding of GIGYF1/2 to the mRNA marks transcripts with perturbed elongation to decay. Our studies reveal how a repressor complex linked to neurological disorders minimizes the protein output of a subset of mRNAs.

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External Sources

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  2. DOI: 10.1016/j.celrep.2020.108262
  3. View record in Web of Science®
  4. WOS: 000579490800020

Library Notes

  1. Fiscal Year: FY2020-2021
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