Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria

It has been debated whether premature ageing in mitochondrial DNA mutator mice is driven by point mutations or deletions of mtDNA. Matic et al generate Mgme1 knockout mice and show here that these mice have tissue-specific replication stalling and accumulate deleted mtDNA, without developing progeri...

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Autores principales: Stanka Matic, Min Jiang, Thomas J. Nicholls, Jay P. Uhler, Caren Dirksen-Schwanenland, Paola Loguercio Polosa, Marie-Lune Simard, Xinping Li, Ilian Atanassov, Oliver Rackham, Aleksandra Filipovska, James B. Stewart, Maria Falkenberg, Nils-Göran Larsson, Dusanka Milenkovic
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Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/e4875b41d2804c3a99656ff7ae1c7aca
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spelling oai:doaj.org-article:e4875b41d2804c3a99656ff7ae1c7aca2021-12-02T14:39:45ZMice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria10.1038/s41467-018-03552-x2041-1723https://doaj.org/article/e4875b41d2804c3a99656ff7ae1c7aca2018-03-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-03552-xhttps://doaj.org/toc/2041-1723It has been debated whether premature ageing in mitochondrial DNA mutator mice is driven by point mutations or deletions of mtDNA. Matic et al generate Mgme1 knockout mice and show here that these mice have tissue-specific replication stalling and accumulate deleted mtDNA, without developing progeria.Stanka MaticMin JiangThomas J. NichollsJay P. UhlerCaren Dirksen-SchwanenlandPaola Loguercio PolosaMarie-Lune SimardXinping LiIlian AtanassovOliver RackhamAleksandra FilipovskaJames B. StewartMaria FalkenbergNils-Göran LarssonDusanka MilenkovicNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-13 (2018)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Stanka Matic
Min Jiang
Thomas J. Nicholls
Jay P. Uhler
Caren Dirksen-Schwanenland
Paola Loguercio Polosa
Marie-Lune Simard
Xinping Li
Ilian Atanassov
Oliver Rackham
Aleksandra Filipovska
James B. Stewart
Maria Falkenberg
Nils-Göran Larsson
Dusanka Milenkovic
Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria
description It has been debated whether premature ageing in mitochondrial DNA mutator mice is driven by point mutations or deletions of mtDNA. Matic et al generate Mgme1 knockout mice and show here that these mice have tissue-specific replication stalling and accumulate deleted mtDNA, without developing progeria.
format article
author Stanka Matic
Min Jiang
Thomas J. Nicholls
Jay P. Uhler
Caren Dirksen-Schwanenland
Paola Loguercio Polosa
Marie-Lune Simard
Xinping Li
Ilian Atanassov
Oliver Rackham
Aleksandra Filipovska
James B. Stewart
Maria Falkenberg
Nils-Göran Larsson
Dusanka Milenkovic
author_facet Stanka Matic
Min Jiang
Thomas J. Nicholls
Jay P. Uhler
Caren Dirksen-Schwanenland
Paola Loguercio Polosa
Marie-Lune Simard
Xinping Li
Ilian Atanassov
Oliver Rackham
Aleksandra Filipovska
James B. Stewart
Maria Falkenberg
Nils-Göran Larsson
Dusanka Milenkovic
author_sort Stanka Matic
title Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria
title_short Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria
title_full Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria
title_fullStr Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria
title_full_unstemmed Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria
title_sort mice lacking the mitochondrial exonuclease mgme1 accumulate mtdna deletions without developing progeria
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/e4875b41d2804c3a99656ff7ae1c7aca
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