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Translation fidelity is critical for protein synthesis and to ensure correct cell functioning. Mutations in the protein synthesis machinery or environmental factors that increase synthesis of mistranslated proteins result in cell death and degeneration and are associated with neurodegenerative diseases, cancer and with an increasing number of mitochondrial disorders. Remarkably, mRNA mistranslation plays critical roles in the evolution of the genetic code, can be beneficial under stress conditions in yeast and in  Escherichia coli  and is an important source of peptides for MHC class I complex in dendritic cells. Despite this, its biology has been overlooked over the years due to technical difficulties in its detection and quantification. In order to shed new light on the biological relevance of mistranslation we have generated codon misreading in  Saccharomyces cerevisiae  using drugs and tRNA engineering methodologies. Surprisingly, such mistranslation up-regulated the longevity gene  PNC1 . Similar results were also obtained in cells grown in the presence of amino acid analogues that promote protein misfolding. The overall data showed that  PNC1  is a biomarker of mRNA mistranslation and protein misfolding and that  PNC1-GFP  fusions can be used to monitor these two important biological phenomena  in vivo  in an easy manner, thus opening new avenues to understand their biological relevance.

The Yeast PNC1 Longevity Gene Is Up-Regulated by mRNA Mistranslation