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Nucleic Acids Res. 2015 Sep 3;43(15):7398-413. doi: 10.1093/nar/gkv692. Epub 2015 Jul 7.

SUV3 helicase is required for correct processing of mitochondrial transcripts.

Author information

1
Division of Metabolic Diseases, Department of Laboratory Medicine; Karolinska Institutet, Stockholm 17177, Sweden.
2
Center for Inherited Metabolic Diseases, Karolinska University Hospital, Stockholm 17176, Sweden.
3
Center for Inherited Metabolic Diseases, Karolinska University Hospital, Stockholm 17176, Sweden Department of Molecular Medicine and Surgery, Science for Life Laboratory, Karolinska Institutet, Stockholm 17176, Sweden.
4
Division of Metabolic Diseases, Department of Laboratory Medicine; Karolinska Institutet, Stockholm 17177, Sweden Center for Inherited Metabolic Diseases, Karolinska University Hospital, Stockholm 17176, Sweden christoph.freyer@ki.se.

Abstract

Mitochondrial gene expression is largely regulated by post-transcriptional mechanisms that control the amount and translation of each mitochondrial mRNA. Despite its importance for mitochondrial function, the mechanisms and proteins involved in mRNA turnover are still not fully characterized. Studies in yeast and human cell lines have indicated that the mitochondrial helicase SUV3, together with the polynucleotide phosphorylase, PNPase, composes the mitochondrial degradosome. To further investigate the in vivo function of SUV3 we disrupted the homolog of SUV3 in Drosophila melanogaster (Dm). Loss of dmsuv3 led to the accumulation of mitochondrial mRNAs, without increasing rRNA levels, de novo transcription or decay intermediates. Furthermore, we observed a severe decrease in mitochondrial tRNAs accompanied by an accumulation of unprocessed precursor transcripts. These processing defects lead to reduced mitochondrial translation and a severe respiratory chain complex deficiency, resulting in a pupal lethal phenotype. In summary, our results propose that SUV3 is predominantly required for the processing of mitochondrial polycistronic transcripts in metazoan and that this function is independent of PNPase.

PMID:
26152302
PMCID:
PMC4551930
DOI:
10.1093/nar/gkv692
[Indexed for MEDLINE]
Free PMC Article

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