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Co-Translational Quality Control Induced by Translational Arrest

Journal

BIOMOLECULES
Volume 13, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/biom13020317

Keywords

quality control; transrational arrest; ribosome collision; ubiquitination; protein degradation; mRNA decay; non-canonical ribosome dissociation

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Genetic mutations, mRNA processing errors, and lack of charged tRNAs can slow down or inhibit translating ribosomes. Monitoring systems are in place to detect and dispose of incomplete nascent chains and aberrant translation products to prevent accumulation and maintain protein homeostasis. Yeast models have been instrumental in uncovering the molecular mechanisms of these co-translational quality control systems.
Genetic mutations, mRNA processing errors, and lack of availability of charged tRNAs sometimes slow down or completely stall translating ribosomes. Since an incomplete nascent chain derived from stalled ribosomes may function anomalously, such as by forming toxic aggregates, surveillance systems monitor every step of translation and dispose of such products to prevent their accumulation. Over the past decade, yeast models with powerful genetics and biochemical techniques have contributed to uncovering the mechanism of the co-translational quality control system, which eliminates the harmful products generated from aberrant translation. We here summarize the current knowledge of the molecular mechanism of the co-translational quality control systems in yeast, which eliminate the incomplete nascent chain, improper mRNAs, and faulty ribosomes to maintain cellular protein homeostasis.

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