Journal
BIOESSAYS
Volume 36, Issue 11, Pages 1024-1031Publisher
WILEY
DOI: 10.1002/bies.201400052
Keywords
DNA; double strand breaks; fragile sites; mitochondria; mitochondrial DNA; replication; single strand breaks
Categories
Funding
- UK Medical Research Council
- European Union
- Academy of Finland
- Sigrid Juselius Foundation
- Tampere University Hospital Medical Research Fund
- MRC [MC_U105663140, MC_UP_1202/14] Funding Source: UKRI
- Medical Research Council [MC_U105663140, MC_UP_1202/14] Funding Source: researchfish
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Last year, we reported a new mechanism of DNA replication in mammals. It occurs inside mitochondria and entails the use of processed transcripts, termed bootlaces, which hybridize with the displaced parental strand as the replication fork advances. Here we discuss possible reasons why such an unusual mechanism of DNA replication might have evolved. The bootlace mechanism can minimize the occurrence and impact of single-strand breaks that would otherwise threaten genome stability. Furthermore, by providing an implicit mismatch recognition system, it should limit the occurrence of replication-dependent deletions and insertions, and defend against invading elements. Such a mechanism may also limit attempts to manipulate the mammalian mitochondrial genome.
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