Editing Mitochondrion (section)

===DNA repair===

Mitochondria can repair oxidative [[DNA damage (naturally occurring)|DNA damage]] by mechanisms analogous to those occurring in the [[cell nucleus]]. The proteins employed in [[mitochondrial DNA|mtDNA]] repair are encoded by nuclear [[gene]]s, and are translocated to the mitochondria. The [[DNA repair]] pathways in mammalian mitochondria include [[base excision repair]], double-strand break repair, direct reversal and [[DNA mismatch repair|mismatch repair]].<ref name="Gredilla-2012">{{cite journal | vauthors = Gredilla R, Garm C, Stevnsner T | title = Nuclear and mitochondrial DNA repair in selected eukaryotic aging model systems | journal = Oxidative Medicine and Cellular Longevity | volume = 2012 | pages = 282438 | date = 2012 | pmid = 23050036 | pmc = 3462412 | doi = 10.1155/2012/282438 | doi-access = free }}</ref><ref name="Saki-2017">{{cite journal | vauthors = Saki M, Prakash A | title = DNA damage related crosstalk between the nucleus and mitochondria | journal = Free Radical Biology & Medicine | volume = 107 | pages = 216–227 | date = June 2017 | pmid = 27915046 | pmc = 5449269 | doi = 10.1016/j.freeradbiomed.2016.11.050 }}</ref> Alternatively, DNA damage may be bypassed, rather than repaired, by translesion synthesis.

Of the several DNA repair process in mitochondria, the base excision repair pathway has been most comprehensively studied.<ref name="Saki-2017" /> Base excision repair is carried out by a sequence of enzyme-catalyzed steps that include recognition and excision of a damaged DNA base, removal of the resulting abasic site, end processing, gap filling and ligation. A common damage in mtDNA that is repaired by base excision repair is [[8-oxoguanine]] produced by oxidation of [[guanine]].<ref name="Leon-2016">{{cite journal | vauthors = Leon J, Sakumi K, Castillo E, Sheng Z, Oka S, Nakabeppu Y | title = 8-Oxoguanine accumulation in mitochondrial DNA causes mitochondrial dysfunction and impairs neuritogenesis in cultured adult mouse cortical neurons under oxidative conditions | journal = Scientific Reports | volume = 6 | pages = 22086 | date = February 2016 | pmid = 26912170 | pmc = 4766534 | doi = 10.1038/srep22086 | bibcode = 2016NatSR...622086L }}</ref>

Double-strand breaks can be repaired by [[homologous recombination]]al repair in both mammalian mtDNA<ref name="Dahal-2018">{{cite journal | vauthors = Dahal S, Dubey S, Raghavan SC | title = Homologous recombination-mediated repair of DNA double-strand breaks operates in mammalian mitochondria | journal = Cellular and Molecular Life Sciences | volume = 75 | issue = 9 | pages = 1641–1655 | date = May 2018 | pmid = 29116362 | pmc = 11105789 | doi = 10.1007/s00018-017-2702-y }}</ref> and plant mtDNA.<ref name="Odahara-2007">{{cite journal | vauthors = Odahara M, Inouye T, Fujita T, Hasebe M, Sekine Y | title = Involvement of mitochondrial-targeted RecA in the repair of mitochondrial DNA in the moss, Physcomitrella patens | journal = Genes & Genetic Systems | volume = 82 | issue = 1 | pages = 43–51 | date = February 2007 | pmid = 17396019 | doi = 10.1266/ggs.82.43 | doi-access = free }}</ref> Double-strand breaks in mtDNA can also be repaired by [[microhomology-mediated end joining]].<ref name="Tadi-2016">{{cite journal | vauthors = Tadi SK, Sebastian R, Dahal S, Babu RK, Choudhary B, Raghavan SC | title = Microhomology-mediated end joining is the principal mediator of double-strand break repair during mitochondrial DNA lesions | journal = Molecular Biology of the Cell | volume = 27 | issue = 2 | pages = 223–235 | date = January 2016 | pmid = 26609070 | pmc = 4713127 | doi = 10.1091/mbc.E15-05-0260 }}</ref> Although there is evidence for the repair processes of direct reversal and mismatch repair in mtDNA, these processes are not well characterized.<ref name="Saki-2017" />