Mitochondrial DNA exhibits resistance to induced point and deletion mutations
Identifieur interne : 000283 ( Main/Exploration ); précédent : 000282; suivant : 000284Mitochondrial DNA exhibits resistance to induced point and deletion mutations
Auteurs : William J. Valente [États-Unis] ; Nolan G. Ericson [États-Unis] ; Alexandra S. Long [Canada] ; Paul A. White [Canada] ; Francesco Marchetti [Canada] ; Jason H. Bielas [États-Unis]Source :
- Nucleic Acids Research [ 0305-1048 ] ; 2016.
Abstract
The accumulation of somatic mitochondrial DNA (mtDNA) mutations contributes to the pathogenesis of human disease. Currently, mitochondrial mutations are largely considered results of inaccurate processing of its heavily damaged genome. However, mainly from a lack of methods to monitor mtDNA mutations with sufficient sensitivity and accuracy, a link between mtDNA damage and mutation has not been established. To test the hypothesis that mtDNA-damaging agents induce mtDNA mutations, we exposed MutaTMMouse mice to benzo[
Url:
DOI: 10.1093/nar/gkw716
PubMed: 27550180
PubMed Central: 5062989
Affiliations:
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Valente</name><affiliation wicri:level="1"><nlm:aff id="AFF1">Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109</wicri:regionArea><wicri:noRegion>WA 98109</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF2">Medical Scientist Training Program, University of Washington School of Medicine, Seattle, WA 98195, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Medical Scientist Training Program, University of Washington School of Medicine, Seattle, WA 98195</wicri:regionArea><wicri:noRegion>WA 98195</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="AFF3">Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195</wicri:regionArea><orgName type="university">Université de Washington</orgName><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation></author><author><name sortKey="Ericson, Nolan G" sort="Ericson, Nolan G" uniqKey="Ericson N" first="Nolan G." last="Ericson">Nolan G. Ericson</name><affiliation wicri:level="1"><nlm:aff id="AFF1">Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109</wicri:regionArea><wicri:noRegion>WA 98109</wicri:noRegion></affiliation></author><author><name sortKey="Long, Alexandra S" sort="Long, Alexandra S" uniqKey="Long A" first="Alexandra S." last="Long">Alexandra S. Long</name><affiliation wicri:level="1"><nlm:aff id="AFF4">Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON K1A 0K9, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON K1A 0K9</wicri:regionArea><wicri:noRegion>ON K1A 0K9</wicri:noRegion></affiliation></author><author><name sortKey="White, Paul A" sort="White, Paul A" uniqKey="White P" first="Paul A." last="White">Paul A. White</name><affiliation wicri:level="1"><nlm:aff id="AFF4">Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON K1A 0K9, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON K1A 0K9</wicri:regionArea><wicri:noRegion>ON K1A 0K9</wicri:noRegion></affiliation></author><author><name sortKey="Marchetti, Francesco" sort="Marchetti, Francesco" uniqKey="Marchetti F" first="Francesco" last="Marchetti">Francesco Marchetti</name><affiliation wicri:level="1"><nlm:aff id="AFF4">Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON K1A 0K9, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON K1A 0K9</wicri:regionArea><wicri:noRegion>ON K1A 0K9</wicri:noRegion></affiliation></author><author><name sortKey="Bielas, Jason H" sort="Bielas, Jason H" uniqKey="Bielas J" first="Jason H." last="Bielas">Jason H. Bielas</name><affiliation wicri:level="1"><nlm:aff id="AFF1">Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Translational Research Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109</wicri:regionArea><wicri:noRegion>WA 98109</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="AFF3">Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Molecular and Cellular Biology Graduate Program, University of Washington, Seattle, WA 98195</wicri:regionArea><orgName type="university">Université de Washington</orgName><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation><affiliation wicri:level="4"><nlm:aff id="AFF5">Department of Pathology, University of Washington, Seattle, WA 98195, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, University of Washington, Seattle, WA 98195</wicri:regionArea><orgName type="university">Université de Washington</orgName><placeName><settlement type="city">Seattle</settlement><region type="state">Washington (État)</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF6">Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Human Biology Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109</wicri:regionArea><wicri:noRegion>WA 98109</wicri:noRegion></affiliation></author></analytic><series><title level="j">Nucleic Acids Research</title><idno type="ISSN">0305-1048</idno><idno type="eISSN">1362-4962</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The accumulation of somatic mitochondrial DNA (mtDNA) mutations contributes to the pathogenesis of human disease. Currently, mitochondrial mutations are largely considered results of inaccurate processing of its heavily damaged genome. However, mainly from a lack of methods to monitor mtDNA mutations with sufficient sensitivity and accuracy, a link between mtDNA damage and mutation has not been established. To test the hypothesis that mtDNA-damaging agents induce mtDNA mutations, we exposed Muta<sup>TM</sup>Mouse mice to benzo[<italic>a</italic>]pyrene (B[a]P) or <italic>N</italic>-ethyl-<italic>N</italic>-nitrosourea (ENU), daily for 28 consecutive days, and quantified mtDNA point and deletion mutations in bone marrow and liver using our newly developed Digital Random Mutation Capture (dRMC) and Digital Deletion Detection (3D) assays. Surprisingly, our results demonstrate mutagen treatment did not increase mitochondrial point or deletion mutation frequencies, despite evidence both compounds increase nuclear DNA mutations and demonstrated B[a]P adduct formation in mtDNA. These findings contradict models of mtDNA mutagenesis that assert the elevated rate of mtDNA mutation stems from damage sensitivity and abridged repair capacity. Rather, our results demonstrate induced mtDNA damage does not readily convert into mutation. These findings suggest robust mitochondrial damage responses repress induced mutations after mutagen exposure.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Schon, E A" uniqKey="Schon E">E.A. Schon</name></author><author><name sortKey="Dimauro, S" uniqKey="Dimauro S">S. DiMauro</name></author><author><name sortKey="Hirano, M" uniqKey="Hirano M">M. Hirano</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bender, A" uniqKey="Bender A">A. Bender</name></author><author><name sortKey="Krishnan, K J" uniqKey="Krishnan K">K.J. Krishnan</name></author><author><name sortKey="Morris, C M" uniqKey="Morris C">C.M. 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Lecrenier</name></author><author><name sortKey="Back, J W" uniqKey="Back J">J.W. Back</name></author><author><name sortKey="Speijer, D" uniqKey="Speijer D">D. Speijer</name></author><author><name sortKey="Foury, F" uniqKey="Foury F">F. Foury</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stumpf, J D" uniqKey="Stumpf J">J.D. Stumpf</name></author><author><name sortKey="Copeland, W C" uniqKey="Copeland W">W.C. Copeland</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kasiviswanathan, R" uniqKey="Kasiviswanathan R">R. Kasiviswanathan</name></author><author><name sortKey="Minko, I G" uniqKey="Minko I">I.G. Minko</name></author><author><name sortKey="Lloyd, R S" uniqKey="Lloyd R">R.S. Lloyd</name></author><author><name sortKey="Copeland, W C" uniqKey="Copeland W">W.C. Copeland</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wallace, D C" uniqKey="Wallace D">D.C. Wallace</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><country name="États-Unis"><noRegion><name sortKey="Valente, William J" sort="Valente, William J" uniqKey="Valente W" first="William J." last="Valente">William J. Valente</name></noRegion><name sortKey="Bielas, Jason H" sort="Bielas, Jason H" uniqKey="Bielas J" first="Jason H." last="Bielas">Jason H. Bielas</name><name sortKey="Bielas, Jason H" sort="Bielas, Jason H" uniqKey="Bielas J" first="Jason H." last="Bielas">Jason H. Bielas</name><name sortKey="Bielas, Jason H" sort="Bielas, Jason H" uniqKey="Bielas J" first="Jason H." last="Bielas">Jason H. Bielas</name><name sortKey="Bielas, Jason H" sort="Bielas, Jason H" uniqKey="Bielas J" first="Jason H." last="Bielas">Jason H. Bielas</name><name sortKey="Ericson, Nolan G" sort="Ericson, Nolan G" uniqKey="Ericson N" first="Nolan G." last="Ericson">Nolan G. Ericson</name><name sortKey="Valente, William J" sort="Valente, William J" uniqKey="Valente W" first="William J." last="Valente">William J. Valente</name><name sortKey="Valente, William J" sort="Valente, William J" uniqKey="Valente W" first="William J." last="Valente">William J. Valente</name></country><country name="Canada"><noRegion><name sortKey="Long, Alexandra S" sort="Long, Alexandra S" uniqKey="Long A" first="Alexandra S." last="Long">Alexandra S. Long</name></noRegion><name sortKey="Marchetti, Francesco" sort="Marchetti, Francesco" uniqKey="Marchetti F" first="Francesco" last="Marchetti">Francesco Marchetti</name><name sortKey="White, Paul A" sort="White, Paul A" uniqKey="White P" first="Paul A." last="White">Paul A. White</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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