Journal
NUCLEIC ACIDS RESEARCH
Volume 48, Issue 20, Pages 11244-11258Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkaa804
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Funding
- Federation of Migros Cooperatives
- ETH Zurich Foundation
- World Food System Center at ETH Zurich
- ETH Zurich
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Deletions in mitochondrial DNA (mtDNA) are associated with diverse human pathologies including cancer, aging and mitochondrial disorders. Large-scale deletions span kilobases in length and the loss of these associated genes contributes to crippled oxidative phosphorylation and overall decline in mitochondrial fitness. There is not a united view for how mtDNA deletions are generated and the molecular mechanisms underlying this process are poorly understood. This review discusses the role of replication and repair in mtDNA deletion formation as well as nucleic acid motifs such as repeats, secondary structures, and DNA damage associated with deletion formation in the mitochondrial genome. We propose that while erroneous replication and repair can separately contribute to deletion formation, crosstalk between these pathways is also involved in generating deletions.
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