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Mitochondrial gene expression is largely controlled through post-transcriptional processes including mitochondrial RNA (mt-RNA) processing, modification, decay, and quality control. Defective mitochondrial gene expression results in mitochondrial oxidative phosphorylation (OXPHOS) deficiency and has been implicated in human disease. To fully understand mitochondrial transcription and RNA processing, we performed RNA-seq analyses of mt-RNAs from the fission yeast RNA-seq analyses show that the abundance of mt-RNAs vary greatly. Analysis of data also reveals mt-RNA processing sites including an unusual RNA cleavage event by mitochondrial tRNA (mt-tRNA) 5'-end processing enzyme RNase P. Additionally, this analysis reveals previously unknown mitochondrial transcripts including the-derived fragment, mitochondrial small RNAs (mitosRNAs) such as mt-tRNA-derived fragments (mt-tRFs) and mt-tRNA halves, and mt-tRNAs marked with 3'-CCACCA/CCACC in Finally, RNA-seq reveals that inactivation of encoding mitochondrial tRNA 3'-end processing enzyme globally impairs mt-tRNA 3'-end processing, inhibits mt-mRNA 5'-end processing, and causes accumulation of unprocessed transcripts, demonstrating the feasibility of using RNA-seq to examine the protein known or predicted to be involved in mt-RNA processing in Our work uncovers the complexity of a fungal mitochondrial transcriptome and provides a framework for future studies of mitochondrial gene expression using as a model system.

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Mitochondrial gene expression is essential for adenosine triphosphate synthesis via oxidative phosphorylation, which is the universal energy currency of cells. Here, we report the identification and characterization of a homologue of Saccharomyces cerevisiae Mtf2 (also called Nam1) in Schizosaccharomyces pombe. The Δmtf2 mutant with the intron-containing mitochondrial DNA (mtDNA) exhibited impaired growth on a rich medium containing the non-fermentable carbon source glycerol, suggesting that mtf2 is involved in mitochondrial function. mtf2 deletion in a mitochondrial intron-containing background resulted in a barely detectable level of the cox1 mRNA and a reduction in the level of the cob1 mRNA, and severely impaired cox1 translation. In contrast, mtf2 deletion in a mitochondrial intron-less background did not affect the levels of cox1 and cob1 mRNAs. However, Cox1 synthesis could not be restored to the control level in the Δmtf2 mutant with intron-less mtDNA. Our results suggest that unlike its counterpart in S. cerevisiae which plays a general role in synthesis of mtDNA-encoded proteins, S. pombe Mtf2 primarily functions in cox1 translation and the effect of mtf2 deletion on splicing of introns in mtDNA is likely due to a deficiency in the synthesis of intron-encoded maturases.

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