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Updated: May 9, 2026

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Published on: October 4, 2018
Interactions between peptidyl tRNA hydrolase homologs and the ribosomal release factor Mrf1 in S. pombe mitochondria
Laurent Dujeancourt1, Ricarda Richter, Zofia M Chrzanowska-Lightowlers
1Centre de Génétique Moléculaire, UPR3404, FRC3115, Avenue de la Terrasse, 91198 Gif-sur-Yvette Cedex, France.
Abstract:
Mitochondrial translation synthesizes key subunits of the respiratory complexes. In Schizosaccharomyces pombe, strains lacking Mrf1, the mitochondrial stop codon recognition factor, are viable, suggesting that other factors can play a role in translation termination. S. pombe contains four predicted peptidyl tRNA hydrolases, two of which (Pth3 and Pth4), have a GGQ motif that is conserved in class I release factors. We show that high dosage of Pth4 can compensate for the absence of Mrf1 and loss of Pth4 exacerbates the lack of Mrf1. Also Pth4 is a component of the mitochondrial ribosome, suggesting that it could help recycling stalled ribosomes.
Insights
In yeast, a protein called Pth4 compensates for the loss of mitochondrial translation termination factor Mrf1. Pth4
Area of Science:
- Mitochondrial biology
- Molecular genetics
- Protein synthesis
Background:
- Mitochondrial translation is essential for producing subunits of respiratory complexes.
- In Schizosaccharomyces pombe, the absence of Mrf1 (mitochondrial stop codon recognition factor) is tolerated, implying alternative termination mechanisms.
- S. pombe possesses four predicted peptidyl-tRNA hydrolases, with Pth3 and Pth4 containing a conserved GGQ motif characteristic of class I release factors.
Purpose of the Study:
- To investigate the role of peptidyl-tRNA hydrolases, specifically Pth4, in mitochondrial translation termination in S. pombe.
- To determine if Pth4 can functionally replace Mrf1 in yeast mitochondrial translation termination.
Main Methods:
- Genetic analysis of S. pombe strains with deletions or high expression of Mrf1 and Pth4.
- Biochemical assays to determine the localization and function of Pth4 within the mitochondrial ribosome.
Main Results:
- High expression of Pth4 rescues the viability of S. pombe lacking Mrf1.
- Deletion of Pth4 worsens the phenotype of Mrf1-deficient strains.
- Pth4 was identified as a component of the mitochondrial ribosome.
Conclusions:
- Pth4 plays a significant role in mitochondrial translation termination in S. pombe, capable of compensating for Mrf1.
- Pth4's association with the mitochondrial ribosome suggests a direct role in ribosome recycling and preventing translation errors.
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