Schizosaccharomyces pombe Ppr10 is required for mitochondrial translation.

FEMS Microbiol Lett

Jiangsu Key Laboratory for Microbes and Functional Genomics, College of Life Sciences, Nanjing Normal University, 1 Wen Yuan Rd, Nanjing, 210023, China.

Published: October 2020

AI Article Synopsis

  • The mitochondrial genome is crucial for encoding components of the OXPHOS system, which is vital for mitochondrial functions.
  • Previous research indicated that deleting the ppr10 gene in Schizosaccharomyces pombe drastically reduces the levels of certain mitochondrial transcripts and translation.
  • In this study, it was found that while deletion of ppr10 does not affect mRNA levels for cox1 and cob1 when mitochondrial introns are absent, it still negatively impacts the synthesis of their corresponding proteins and cannot correct the respiratory growth defect caused by this deletion.

Article Abstract

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.

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Source
http://dx.doi.org/10.1093/femsle/fnaa170DOI Listing

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