In a study published in PNAS, the team led by Prof. Zhou Xiaolong and Prof. Wang Enduo from the Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences report that mammalian mitochondrial translation requires a high-level of accuracy at Thr codons, which is mediated by the proofreading (editing) function of mitochondrial threonyl-tRNA synthetase (mtThrRS).
, the team led by Prof. Zhou Xiaolong and Prof. Wang Enduo from the Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences report that mammalian mitochondrial translation requires a high-level of accuracy at Thr codons, which is mediated by the proofreading function of mitochondrial threonyl-tRNA synthetase .
Mitochondrion is one of the most crucial organelles in eukaryotes, regulating multiple cellular functions, such as, redox homeostasis, calcium uptake and extrusion, and cell fate. Mammalian mitochondrion harbors its own genome , encoding 22 tRNAs, two rRNAs and 13 proteins, which are all essential subunits of respiratory complexes.
Aminoacyl-tRNA synthetases ensure both speed and accuracy of mRNA translation by catalyzing tRNA aminoacylation. About half of aaRSs evolve an additional editing function to clear mischarged tRNAs to avoid mRNA mistranslation. Loss of editing of cytoplasmic aaRSs causes neurodegeneration. However, most mitochondrial aaRSs have lost editing domains during evolution. Only four mitochondrial aaRSs retain an intact editing domain. Whether such a simple mitochondrial translation with only 3,789 codons needs translational quality control remains unclear.
In this study, the researchers found that mtThrRS possesses editing capability to hydrolyze mischarged Ser-tRNAin vitro.
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