Editing Genetic recombination (section)

==Recombinational repair==
DNA damages caused by a variety of exogenous agents (e.g. [[Ultraviolet|UV light]], [[X-ray]]s, chemical [[cross-link]]ing agents) can be repaired by homologous recombinational repair (HRR).<ref name="pmid825857">{{cite journal | vauthors = Baker BS, Boyd JB, Carpenter AT, Green MM, Nguyen TD, Ripoll P, Smith PD | title = Genetic controls of meiotic recombination and somatic DNA metabolism in Drosophila melanogaster | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 73 | issue = 11 | pages = 4140–4 | date = November 1976 | pmid = 825857 | pmc = 431359 | doi = 10.1073/pnas.73.11.4140 | bibcode = 1976PNAS...73.4140B | doi-access = free }}</ref><ref>{{cite book | vauthors = Boyd JB | date = 1978 | chapter = DNA repair in ''Drosophila'' | title = DNA Repair Mechanisms | veditors = Hanawalt PC, Friedberg EC, Fox CF | pages = 449–452 | publisher = Academic Press | location = New York }}</ref>  These findings suggest that [[DNA damage (naturally occurring)|DNA damages arising from natural processes]], such as exposure to reactive oxygen species that are byproducts of normal metabolism, are also repaired by HRR. In humans, deficiencies in the gene products necessary for HRR during meiosis likely cause infertility<ref name="pmid17177185">{{cite journal | vauthors = Galetzka D, Weis E, Kohlschmidt N, Bitz O, Stein R, Haaf T | title = Expression of somatic DNA repair genes in human testes | journal = Journal of Cellular Biochemistry | volume = 100 | issue = 5 | pages = 1232–9 | date = April 2007 | pmid = 17177185 | doi = 10.1002/jcb.21113 | s2cid = 23743474 }}</ref>  In humans, deficiencies in gene products necessary for HRR, such as [[BRCA1]] and [[BRCA2]], increase the risk of cancer (see [[DNA repair-deficiency disorder]]).

In bacteria, transformation is a process of gene transfer that ordinarily occurs between individual cells of the same bacterial species. Transformation involves integration of donor DNA into the recipient chromosome by recombination. This process appears to be an adaptation for repairing DNA damages in the recipient chromosome by HRR.<ref name=Michod>{{cite journal | vauthors = Michod RE, Bernstein H, Nedelcu AM | title = Adaptive value of sex in microbial pathogens | journal = Infection, Genetics and Evolution | volume = 8 | issue = 3 | pages = 267–85 | date = May 2008 | pmid = 18295550 | doi = 10.1016/j.meegid.2008.01.002 | bibcode = 2008InfGE...8..267M | url = http://www.hummingbirds.arizona.edu/Faculty/Michod/Downloads/IGE%20review%20sex.pdf }}</ref>  Transformation may provide a benefit to pathogenic bacteria by allowing repair of DNA damage, particularly damages that occur in the inflammatory, oxidizing environment associated with infection of a host.

When two or more viruses, each containing lethal genomic damages, infect the same host cell, the virus genomes can often pair with each other and undergo HRR to produce viable progeny. This process, referred to as multiplicity reactivation, has been studied in lambda and [[T4 bacteriophage]]s,<ref>{{cite journal | vauthors = Bernstein C | title = Deoxyribonucleic acid repair in bacteriophage | journal = Microbiological Reviews | volume = 45 | issue = 1 | pages = 72–98 | date = March 1981 | pmid = 6261109 | pmc = 281499 | doi = 10.1128/MMBR.45.1.72-98.1981 }}</ref> as well as in several pathogenic viruses. In the case of pathogenic viruses, multiplicity reactivation may be an adaptive benefit to the virus since it allows the repair of DNA damages caused by exposure to the oxidizing environment produced during host infection.<ref name=Michod /> See also [[reassortment]].