Editing Mitosis (section)

===Mitotic recombination===

Mitotic cells irradiated with [[X-ray]]s in the [[G1 phase]] of the [[cell cycle]] repair recombinogenic [[DNA damage (naturally occurring)|DNA damages]] primarily by [[Homologous recombination|recombination]] between [[homologous chromosome]]s.<ref name="Kadyk-1992">{{cite journal | vauthors = Kadyk LC, Hartwell LH | title = Sister chromatids are preferred over homologs as substrates for recombinational repair in Saccharomyces cerevisiae | journal = Genetics | volume = 132 | issue = 2 | pages = 387–402 | date = October 1992 | doi = 10.1093/genetics/132.2.387 | pmid = 1427035 | pmc = 1205144 }}</ref>   Mitotic cells irradiated in the [[G2 phase]] repair such damages preferentially by [[sister chromatid exchange|sister-chromatid recombination]].<ref name="Kadyk-1992" />  [[Mutation]]s in [[gene]]s encoding enzymes employed in recombination cause cells to have increased sensitivity to being killed by a variety of DNA damaging agents.<ref>{{cite journal | vauthors = Botthof JG, Bielczyk-Maczyńska E, Ferreira L, Cvejic A | title = rad51 leads to Fanconi anemia-like symptoms in zebrafish | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 114 | issue = 22 | pages = E4452–E4461 | date = May 2017 | pmid = 28512217 | pmc = 5465903 | doi = 10.1073/pnas.1620631114 | quote = Here we provide in vivo evidence that the decrease in HSPC numbers in adult fish indeed stems from a combination of decreased proliferation and increased apoptosis during embryonic development. This defect appears to be mediated via p53(10), as our p53/rad51 double mutants did not display any observable hematological defects in embryos or adults. | doi-access = free }}</ref><ref>{{cite journal | vauthors = Stürzbecher HW, Donzelmann B, Henning W, Knippschild U, Buchhop S | title = p53 is linked directly to homologous recombination processes via RAD51/RecA protein interaction | journal = The EMBO Journal | volume = 15 | issue = 8 | pages = 1992–2002 | date = April 1996 | pmid = 8617246 | pmc = 450118 | doi = 10.1002/j.1460-2075.1996.tb00550.x }}</ref><ref>{{cite journal | vauthors = Sonoda E, Sasaki MS, Buerstedde JM, Bezzubova O, Shinohara A, Ogawa H, Takata M, Yamaguchi-Iwai Y, Takeda S | display-authors = 6 | title = Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death | journal = The EMBO Journal | volume = 17 | issue = 2 | pages = 598–608 | date = January 1998 | pmid = 9430650 | pmc = 1170409 | doi = 10.1093/emboj/17.2.598 }}</ref> These findings suggest that mitotic recombination is an adaptation for repairing DNA damages including those that are potentially lethal.