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

Abstract

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.