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Journal Article

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

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Weber,  R
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons272043

Chung,  M-Y
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons272046

Keskeny,  C
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons272049

Valkov,  E
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons271767

Izaurralde,  E
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;

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Igreja,  C
Department Biochemistry, Max Planck Institute for Developmental Biology, Max Planck Society;
Regulation and Post-Translational Modification of Gene Expression in Nematodes Group, Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Citation

Weber, R., Chung, M.-Y., Keskeny, C., Zinnall, U., Landthaler, M., Valkov, E., et al. (2020). 4EHP and GIGYF1/2 Mediate Translation-Coupled Messenger RNA Decay. Cell Reports, 33(2): 108262. doi:10.1016/j.celrep.2020.108262.


Cite as: https://hdl.handle.net/21.11116/0000-000A-3D29-5
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.