266:, which plays a role in DNA replication and repair. This mutation leads to high rates of mitotic recombination in mice, and this recombination rate is in turn responsible for causing tumor susceptibility in those mice. At the same time, mitotic recombination may be beneficial: it may play an important role in repairing double stranded breaks, and it may be beneficial to the organism if having homozygous dominant alleles is more functional than the heterozygous state. For use in experimentation with genomes in model organisms such as
90:
115:. If the chromatids containing different alleles line up on the same side of the plate, then the resulting daughter cells will appear heterozygous and be undetectable, despite the crossover event. However, if chromatids containing the same alleles line up on the same side, the daughter cells will be homozygous at that locus. This results in
226:
form a double
Holliday junction at a common repeat site and are later sheared in such a way that they switch places. In either model, the chromosomes are not guaranteed to trade evenly, or even to rejoin on opposite sides thus most patterns of cleavage do not result in any crossover event. Uneven
85:
as early as 1925, but it was only in 1936 that Curt Stern explained it as a result of mitotic recombination. Prior to Stern's work, it was hypothesized that twin spotting happened because certain genes had the ability to eliminate the chromosome on which they were located. Later experiments
126:. It has been suggested that recombination takes place during G1, when the DNA is in its 2-strand phase, and replicated during DNA synthesis. It is also possible to have the DNA break leading to mitotic recombination happen during G1, but for the repair to happen after replication.
629:
Haynes, R.H. & Kunz, B.A. (1981). DNA repair and mutagenesis in yeast. In: Strathern, J; Jones, E; Broach J. editors. The
Molecular Biology of the Yeast Saccharomyces. Life Cycle and Inheritance. Cold Spring Harbor, N.Y., Cold Spring Harbor Laboratory,
119:, where one cell presents the homozygous recessive phenotype and the other cell has the homozygous wild type phenotype. If those daughter cells go on to replicate and divide, the twin spots will continue to grow and reflect the differential phenotype.
102:
Mitotic recombination can happen at any locus but is observable in individuals that are heterozygous at a given locus. If a crossover event between non-sister chromatids affects that locus, then both homologous chromosomes will have one
254:, some asexually reproducing fungi and in normal human cells, where the event may allow normally recessive cancer-causing alleles to be expressed and thus predispose the cell in which it occurs to the development of
58:
subsequent to replication (but prior to cell division). Inter-sister homologous recombination is ordinarily genetically silent. During mitosis the incidence of recombination between non-sister homologous
182:
The mechanisms behind mitotic recombination are similar to those behind meiotic recombination. These include sister chromatid exchange and mechanisms related to DNA double strand break repair by
230:
Alternatively, a crossover can occur during DNA repair if, due to extensive damage, the homologous chromosome is chosen to be the template over the sister chromatid. This leads to
234:
since one copy of the allele is copied across from the homologous chromosome and then synthesized into the breach on the damaged chromosome. The net effect of this would be one
1015:
214:
There are several theories on how mitotic crossover occurs. In the simple crossover model, the two homologous chromosomes overlap on or near a common
38:
because it is the only source of recombination within an individual. Additionally, mitotic recombination can result in the expression of recessive
860:
222:, which is then repaired using one of the two strands. This can lead to the two chromatids switching places. In another model, two overlapping
140:, mutations in several genes needed for mitotic (and meiotic) recombination cause increased sensitivity to inactivation by radiation and/or
171:
258:. Alternately, a cell may become a homozygous mutant for a tumor-suppressing gene, leading to the same result. For example,
525:
Lee, Phoebe S.; Greenwell, Patricia W.; Dominska, Margaret; Gawel, Malgorzata; Hamilton, Monica; Petes, Thomas D. (2009).
202:
intermediate or SDSA. In addition, non-homologous mitotic recombination is a possibility and can often be attributed to
34:
in both sexual and asexual organisms. In asexual organisms, the study of mitotic recombination is one way to understand
1020:
1010:
915:
Luo, Guangbin; et al. (2000). "Cancer predisposition caused by elevated mitotic recombination in Bloom mice".
203:
646:
2 gene is required for homothallic interconversion of mating types and spontaneous mitotic recombination in yeast"
215:
183:
136:
51:
187:
268:
159:
77:
86:
uncovered when mitotic recombination occurs in the cell cycle and the mechanisms behind recombination.
958:
Xu, T; GM Rubin (April 1993). "Analysis of genetic mosaics in developing and adult
Drosophila tissues".
273:
170:-plus-UV light, suggesting that mitotic recombinational repair is required for removal of the different
23:
89:
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259:
219:
163:
72:
993:
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527:"A Fine-Structure Map of Spontaneous Mitotic Crossovers in the Yeast Saccharomyces cerevisiae"
504:
445:
396:
347:
199:
55:
752:
Helleday, Thomas (2003). "Pathways for
Mitotic Homologous Recombination in Mammalian Cells".
967:
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337:
329:
367:"Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis"
318:"Loss of Heterozygosity, or: How I learned to Stop Worrying and Love Mitotic Recombination"
195:
112:
35:
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Mitotic recombination can result in homozygous expression in a heterozygous individual
1004:
817:
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263:
47:
27:
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808:
235:
141:
43:
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465:"Evidence that Spontaneous Mitotic Recombination Occurs at the Two-Strand Stage"
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104:
60:
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842:"Double-Strand Break Repair via Double Holliday Junctions (Szostak Model)"
689:
670:
351:
508:
227:
trading introduces many of the deleterious effects of mitotic crossover.
150:
is required for mitotic recombination as well as meiotic recombination.
46:
individual. This expression has important implications for the study of
789:"Multiple Pathways of Recombination Induced by Double-Strand Breaks in
31:
705:"The Role of Radiation (rad) Genes in Meiotic Recombination in Yeast"
255:
39:
382:
111:
of the daughter cells depends on how the chromosomes line up on the
71:
The discovery of mitotic recombination came from the observation of
333:
928:
861:"Pathways for mitotic homologous recombination in mammalian cells"
416:"Somatic Crossing Over and Segregation in Drosophila Melanogaster"
155:
146:
88:
191:
154:
mutant yeast cells have increased sensitivity to killing by
81:. This twin spotting, or mosaic spotting, was observed in
469:
Proceedings of the
National Academy of Sciences of the USA
272:, mitotic recombination can be induced via X-ray and the
703:
Game JC, Zamb TJ, Braun RJ, Resnick M, Roth RM (1980).
63:
is only about 1% of that between sister chromatids.
581:"Mitotic Recombination: Why? When? How? Where?"
296:Hartl, Daniel L. and Maryellen Ruvolo (2012).
8:
311:
309:
307:
797:Microbiology and Molecular Biology Reviews
298:Genetics: Analysis of Genetics and Genomes
816:
787:Pâques, Frédéric; James E. Haber (1999).
728:
679:
669:
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552:
542:
498:
488:
439:
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122:Mitotic recombination takes place during
107:containing each genotype. The resulting
574:
572:
291:
289:
190:, synthesis-dependent strand annealing (
285:
250:Mitotic crossover is known to occur in
463:Esposito, Michael S (September 1978).
50:and lethal recessive alleles. Mitotic
859:Helleday, Thomas (27 November 2003).
520:
518:
7:
316:Tischfield, Jay A. (November 1997).
1016:Modification of genetic information
300:. Burlington: Jones & Bartlett.
322:American Journal of Human Genetics
14:
640:Malone RE, Esposito RE (1980).
579:LaFave, MC; J Sekelsky (2009).
809:10.1128/MMBR.63.2.349-404.1999
1:
365:Moynahan ME, Jasin M (2010).
30:during their preparation for
16:Type of genetic recombination
997:. W. H. Freeman and Company.
880:10.1016/j.mrfmmm.2003.08.013
766:10.1016/j.mrfmmm.2003.08.013
650:Proc. Natl. Acad. Sci. U.S.A
598:10.1371/journal.pgen.1000411
544:10.1371/journal.pgen.1000410
246:Advantages and disadvantages
262:is caused by a mutation in
1037:
204:non-homologous end joining
432:10.1093/genetics/21.6.625
791:Saccharomyces cerevisiae
721:10.1093/genetics/94.1.51
371:Nat. Rev. Mol. Cell Biol
216:Chromosomal fragile site
200:double-Holliday Junction
184:homologous recombination
174:caused by these agents.
137:Saccharomyces cerevisiae
52:homologous recombination
994:Modern Genetic Analysis
991:Griffiths et al. 1999.
269:Drosophila melanogaster
218:(CFS). This leads to a
188:single-strand annealing
160:methyl methanesulfonate
78:Drosophila melanogaster
972:10.1242/dev.117.4.1223
490:10.1073/pnas.75.9.4436
130:Response to DNA damage
94:
54:occurs mainly between
671:10.1073/pnas.77.1.503
274:FLP-FRT recombination
144:. For example, gene
134:In the budding yeast
92:
24:genetic recombination
20:Mitotic recombination
414:Stern, Curt (1936).
662:1980PNAS...77..503M
481:1978PNAS...75.4436E
238:chromosome and one
220:double-strand break
142:genotoxic chemicals
1021:Molecular genetics
1011:Cellular processes
95:
26:that may occur in
966:(4): 1223–12237.
868:Mutation Research
754:Mutation Research
224:sister chromatids
168:8-methoxypsoralen
56:sister chromatids
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260:Bloom's syndrome
164:DNA crosslinking
42:in an otherwise
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383:10.1038/nrm2851
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252:D. melanogaster
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196:gene conversion
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113:metaphase plate
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83:D. melanogaster
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36:genetic linkage
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897:on 24 May 2014
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232:gene synthesis
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73:twin spotting
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48:tumorigenesis
45:
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242:chromosome.
236:heterozygous
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101:
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44:heterozygous
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960:Development
172:DNA damages
1005:Categories
901:2012-12-26
585:PLOS Genet
531:PLOS Genet
280:References
240:homozygous
198:through a
178:Mechanisms
124:interphase
98:Occurrence
61:chromatids
846:Animation
109:phenotype
105:chromatid
67:Discovery
945:21218975
937:11101838
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709:Genetics
630:371-414.
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276:system.
186:such as
162:and the
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194:), and
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166:agent
156:X-rays
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735:PMID
686:PMID
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613:PMID
559:PMID
505:PMID
446:PMID
397:PMID
348:PMID
192:SDSA
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