Mitochondrial translational defect extends lifespan in C. elegans by activating UPRmt

To study the function of mitochondrial tars-1 (representing the ORF encoding CeThrRS-1), we used CRISPR–Cas9 to generate a mitochondrial tars-1 knockdown strain of C. elegans named tars-1(ora1) Ⅱ by mutating the start codon “ATG1” to “ACG1”, and the stain was confirmed by whole-exome sequencing.To study the mechanism of abnormal phenotypes in tars-1(ora1) Ⅱ, RNA-Seq was performed. We performed quantitative proteomics by LC–MS/MS to detect the protein abundance in N2 and tars-1(ora1) Ⅱ. Mitochondrial and cytosolic translation are dynamically regulated in a synchronized manner .