Article
Defects in mtDNA replication challenge nuclear genome stability through nucleotide depletion and provide a unifying mechanism for mouse progerias.
Nature metabolism - 1 Oct 2019
Hämäläinen Riikka H, Landoni Juan C, Ahlqvist Kati J, Goffart Steffi, Ryytty Sanna, Rahman M Obaidur, Brilhante Virginia, Icay Katherine, Hautaniemi Sampsa, Wang Liya, Laiho Marikki, Suomalainen Anu
Abstract excerpt
Mitochondrial DNA (mtDNA) mutagenesis and nuclear DNA repair defects are considered cellular mechanisms of ageing. mtDNA mutator mice with increased mtDNA mutagenesis show signs of premature ageing. However, why patients with mitochondrial diseases, or mice with other forms of mitochondrial dysfunction, do not age prematurely remains unknown. Here, we show that cells from mutator mice display challenged nuclear...
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