Abstract
Mitochondrial genomes in flowering plants differ from those in animals and yeasts in several ways, including having large and variable sizes, circular, linear and branched structures, long repeat sequences that participate in homologous recombinations, and variable genes orders, even within a species. Understanding these differences has been hampered by a lack of genetic methods for transforming plant mitochondrial genomes. We recently succeeded in disrupting targeted genes in mitochondrial genomes by mitochondria-targeted transcription activator-like effector nucleases (mitoTALENs) in rice, rapeseed, and Arabidopsis. Double-strand breaks created by mitoTALENs were repaired not by non-homologous end-joining (NHEJ) but by homologous recombination (HR) between repeats near and far from the target sites, resulting in new genomic structures with large deletions and different configurations. On the other hand, in mammals, TALENs-induced DSBs cause small insertions or deletions in nuclear genomes and degradation of mitochondrial genomes. These results suggest that the mitochondrial and nuclear genomes of plants and mammals have distinct mechanisms for responding to naturally occurring DSBs. The different responses appear to be well suited to differences in size and copy numbers of each genome.
Highlights
Mitochondria, in addition to generating cellular energy in the form of ATP through oxidative phosphorylation, produce reactive oxygen species that cause double-strand breaks (DSBs) in the mitochondrial DNA
DSBs in mitochondrial DNAs can be created by replication errors [1,2]
DSBs are mainly repaired by two mechanisms, homologous recombination (HR) and non-homologous end joining (NHEJ)
Summary
Mitochondria, in addition to generating cellular energy in the form of ATP through oxidative phosphorylation, produce reactive oxygen species that cause double-strand breaks (DSBs) in the mitochondrial DNA. DSBs in mitochondrial DNAs can be created by replication errors [1,2]. DSBs of DNA can be severely damaging, so organisms have developed mechanisms for repairing them.
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