Mitochondrial translational defect extends lifespan in C. elegans by activating UPRmt
Published: 6 September 2022| Version 1 | DOI: 10.17632/tzyy8gb9x3.1
Contributor:
Chang ChenDescription
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 .
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Institutions
Institute of Biophysics Chinese Academy of Sciences
Categories
Proteomics, RNA Sequencing