Schizosaccharomyces pombe Ppr10 is required for mitochondrial translation.
Schizosaccharomyces pombe
OXPHOS
PPR protein
intron splicing
mitochondria
translation
Journal
FEMS microbiology letters
ISSN: 1574-6968
Titre abrégé: FEMS Microbiol Lett
Pays: England
ID NLM: 7705721
Informations de publication
Date de publication:
21 10 2020
21 10 2020
Historique:
received:
18
07
2020
accepted:
10
10
2020
pubmed:
14
10
2020
medline:
22
7
2021
entrez:
13
10
2020
Statut:
ppublish
Résumé
The mitochondrial genome encodes key components of the oxidative phosphorylation (OXPHOS) system, whose expression is essential for mitochondrial functions. We have previously shown that deletion of the Schizosaccharomyces pombe ppr10 encoding a pentatricopeptide repeat protein severely reduces the mature levels of intron-containing mitochondrial transcripts cox1 and cob1, and severely impairs mitochondrial translation. In this study, we examined the possibility that the reduced levels of Cox1 and Cob1 proteins in cells were due to lowered levels of cox1 and cob1 mRNAs. We found that deletion of ppr10 did not affect the levels of mature cox1 and cob1 mRNAs in a mitochondrial intronless background. However, synthesis of Cox1 and Cob1 proteins were still severely affected by deletion of ppr10 in a mitochondrial intronless background. Consistent with this, we found that deletion of mitochondrial introns could not rescue the respiratory growth defect of Δppr10 cells. Our results reveal that Ppr10 is not required for the stability of cox1 and cob1 mRNAs, and provide further support for the idea that Ppr10 plays a critical role in mitochondrial translation.
Identifiants
pubmed: 33049028
pii: 5922721
doi: 10.1093/femsle/fnaa170
pii:
doi:
Substances chimiques
Ppr10 protein, S pombe
0
RNA-Binding Proteins
0
Schizosaccharomyces pombe Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of FEMS.