POLRMT regulates the switch between replication primer formation and gene expression of mammalian mtDNA.
Identifieur interne : 001A97 ( PubMed/Corpus ); précédent : 001A96; suivant : 001A98POLRMT regulates the switch between replication primer formation and gene expression of mammalian mtDNA.
Auteurs : Inge Kühl ; Maria Miranda ; Viktor Posse ; Dusanka Milenkovic ; Arnaud Mourier ; Stefan J. Siira ; Nina A. Bonekamp ; Ulla Neumann ; Aleksandra Filipovska ; Paola Loguercio Polosa ; Claes M. Gustafsson ; Nils-Göran LarssonSource :
- Science advances [ 2375-2548 ] ; 2016.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : DNA, Mitochondrial, DNA-Binding Proteins, DNA-Directed RNA Polymerases, High Mobility Group Proteins.
- genetics : DNA Replication.
- Animals, Gene Expression Regulation, Genome, Mitochondrial, Mice, Transcription, Genetic.
Abstract
Mitochondria are vital in providing cellular energy via their oxidative phosphorylation system, which requires the coordinated expression of genes encoded by both the nuclear and mitochondrial genomes (mtDNA). Transcription of the circular mammalian mtDNA depends on a single mitochondrial RNA polymerase (POLRMT). Although the transcription initiation process is well understood, it is debated whether POLRMT also serves as the primase for the initiation of mtDNA replication. In the nucleus, the RNA polymerases needed for gene expression have no such role. Conditional knockout of Polrmt in the heart results in severe mitochondrial dysfunction causing dilated cardiomyopathy in young mice. We further studied the molecular consequences of different expression levels of POLRMT and found that POLRMT is essential for primer synthesis to initiate mtDNA replication in vivo. Furthermore, transcription initiation for primer formation has priority over gene expression. Surprisingly, mitochondrial transcription factor A (TFAM) exists in an mtDNA-free pool in the Polrmt knockout mice. TFAM levels remain unchanged despite strong mtDNA depletion, and TFAM is thus protected from degradation of the AAA(+) Lon protease in the absence of POLRMT. Last, we report that mitochondrial transcription elongation factor may compensate for a partial depletion of POLRMT in heterozygous Polrmt knockout mice, indicating a direct regulatory role of this factor in transcription. In conclusion, we present in vivo evidence that POLRMT has a key regulatory role in the replication of mammalian mtDNA and is part of a transcriptional mechanism that provides a switch between primer formation for mtDNA replication and mitochondrial gene expression.
DOI: 10.1126/sciadv.1600963
PubMed: 27532055
Links to Exploration step
pubmed:27532055Le document en format XML
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<term>DNA-Directed RNA Polymerases (genetics)</term>
<term>Gene Expression Regulation</term>
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<front><div type="abstract" xml:lang="en">Mitochondria are vital in providing cellular energy via their oxidative phosphorylation system, which requires the coordinated expression of genes encoded by both the nuclear and mitochondrial genomes (mtDNA). Transcription of the circular mammalian mtDNA depends on a single mitochondrial RNA polymerase (POLRMT). Although the transcription initiation process is well understood, it is debated whether POLRMT also serves as the primase for the initiation of mtDNA replication. In the nucleus, the RNA polymerases needed for gene expression have no such role. Conditional knockout of Polrmt in the heart results in severe mitochondrial dysfunction causing dilated cardiomyopathy in young mice. We further studied the molecular consequences of different expression levels of POLRMT and found that POLRMT is essential for primer synthesis to initiate mtDNA replication in vivo. Furthermore, transcription initiation for primer formation has priority over gene expression. Surprisingly, mitochondrial transcription factor A (TFAM) exists in an mtDNA-free pool in the Polrmt knockout mice. TFAM levels remain unchanged despite strong mtDNA depletion, and TFAM is thus protected from degradation of the AAA(+) Lon protease in the absence of POLRMT. Last, we report that mitochondrial transcription elongation factor may compensate for a partial depletion of POLRMT in heterozygous Polrmt knockout mice, indicating a direct regulatory role of this factor in transcription. In conclusion, we present in vivo evidence that POLRMT has a key regulatory role in the replication of mammalian mtDNA and is part of a transcriptional mechanism that provides a switch between primer formation for mtDNA replication and mitochondrial gene expression.</div>
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<Abstract><AbstractText>Mitochondria are vital in providing cellular energy via their oxidative phosphorylation system, which requires the coordinated expression of genes encoded by both the nuclear and mitochondrial genomes (mtDNA). Transcription of the circular mammalian mtDNA depends on a single mitochondrial RNA polymerase (POLRMT). Although the transcription initiation process is well understood, it is debated whether POLRMT also serves as the primase for the initiation of mtDNA replication. In the nucleus, the RNA polymerases needed for gene expression have no such role. Conditional knockout of Polrmt in the heart results in severe mitochondrial dysfunction causing dilated cardiomyopathy in young mice. We further studied the molecular consequences of different expression levels of POLRMT and found that POLRMT is essential for primer synthesis to initiate mtDNA replication in vivo. Furthermore, transcription initiation for primer formation has priority over gene expression. Surprisingly, mitochondrial transcription factor A (TFAM) exists in an mtDNA-free pool in the Polrmt knockout mice. TFAM levels remain unchanged despite strong mtDNA depletion, and TFAM is thus protected from degradation of the AAA(+) Lon protease in the absence of POLRMT. Last, we report that mitochondrial transcription elongation factor may compensate for a partial depletion of POLRMT in heterozygous Polrmt knockout mice, indicating a direct regulatory role of this factor in transcription. In conclusion, we present in vivo evidence that POLRMT has a key regulatory role in the replication of mammalian mtDNA and is part of a transcriptional mechanism that provides a switch between primer formation for mtDNA replication and mitochondrial gene expression.</AbstractText>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
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<MeshHeading><DescriptorName UI="D004261" MajorTopicYN="N">DNA Replication</DescriptorName>
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<MeshHeading><DescriptorName UI="D004272" MajorTopicYN="N">DNA, Mitochondrial</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D004268" MajorTopicYN="N">DNA-Binding Proteins</DescriptorName>
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<MeshHeading><DescriptorName UI="D012321" MajorTopicYN="N">DNA-Directed RNA Polymerases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
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<MeshHeading><DescriptorName UI="D054629" MajorTopicYN="N">Genome, Mitochondrial</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006609" MajorTopicYN="N">High Mobility Group Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
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<MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName>
</MeshHeading>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">7S RNA</Keyword>
<Keyword MajorTopicYN="Y">Mitochondria</Keyword>
<Keyword MajorTopicYN="Y">POLRMT knockout mouse</Keyword>
<Keyword MajorTopicYN="Y">light strand promoter</Keyword>
<Keyword MajorTopicYN="Y">mitochondrial RNA polymerase</Keyword>
<Keyword MajorTopicYN="Y">mitochondrial gene expression</Keyword>
<Keyword MajorTopicYN="Y">mtDNA</Keyword>
<Keyword MajorTopicYN="Y">mtDNA replication</Keyword>
<Keyword MajorTopicYN="Y">mtDNA-free TFAM pool</Keyword>
<Keyword MajorTopicYN="Y">twinkle</Keyword>
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<Day>02</Day>
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<Month>07</Month>
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