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Journal articles on the topic 'Illegitimate recombination'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Ehrlich, S. D., H. Bierne, E. d'Alençon, D. Vilette, M. Petranovic, P. Noirot, and B. Michel. "Mechanisms of illegitimate recombination." Gene 135, no. 1-2 (December 1993): 161–66. http://dx.doi.org/10.1016/0378-1119(93)90061-7.

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2

Shiraishi, Kouya, Katsuhiro Hanada, Yoichiro Iwakura, and Hideo Ikeda. "Roles of RecJ, RecO, and RecR in RecET-Mediated Illegitimate Recombination in Escherichia coli." Journal of Bacteriology 184, no. 17 (September 1, 2002): 4715–21. http://dx.doi.org/10.1128/jb.184.17.4715-4721.2002.

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ABSTRACT We analyzed effects of overexpression of RecE and RecT on illegitimate recombination during prophage induction in Escherichia coli and found that frequencies of spontaneous and UV-induced illegitimate recombination are enhanced by coexpression of RecE and RecT in the wild type, but the enhanced recombination was reduced by recJ, recO, or recR mutation. The results indicated that RecET-mediated illegitimate recombination depends on the functions of RecJ, RecO, and RecR, suggesting that the RecE and RecJ exonucleases play different roles in this recombination pathway and that the RecO and RecR proteins also play important roles in the recombination. On the other hand, the frequency of the RecET-mediated illegitimate recombination was enhanced by a recQ mutation, implying that the RecQ protein plays a role in suppression of RecET-mediated illegitimate recombination. It was also found that RecET-mediated illegitimate recombination is independent of the RecA function with UV irradiation, but it is enhanced by the recA mutation without UV irradiation. Based on these results, we propose a model for the roles of RecJOR on RecET-mediated illegitimate recombination.

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3

Yamashita, Teruhito, Katsuhiro Hanada, Mihoko Iwasaki, Hirotaka Yamaguchi, and Hideo Ikeda. "Illegitimate Recombination Induced by Overproduction of DnaB Helicase in Escherichia coli." Journal of Bacteriology 181, no. 15 (August 1, 1999): 4549–53. http://dx.doi.org/10.1128/jb.181.15.4549-4553.1999.

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ABSTRACT Illegitimate recombination that usually takes place at a low frequency is greatly enhanced by treatment with DNA-damaging agents. It is thought that DNA double-strand breaks induced by this DNA damage are important for initiation of illegitimate recombination. Here we show that illegitimate recombination is enhanced by overexpression of the DnaB protein in Escherichia coli. The recombination enhanced by DnaB overexpression occurred between short regions of homology. We propose a model for the initiation of illegitimate recombination in which DnaB overexpression may excessively unwind DNA at replication forks and induce double-strand breaks, resulting in illegitimate recombination. The defect in RecQ has a synergistic effect on the increased illegitimate recombination in cells containing the overproduced DnaB protein, implying that DnaB works in the same pathway as RecQ does but that they work at different steps.

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4

DUESBERG, PETER H., REN-PING ZHOU, and DAVID GOODRICH. "Cancer Genes by Illegitimate Recombination." Annals of the New York Academy of Sciences 567, no. 1 Viral Oncogen (August 1989): 259–73. http://dx.doi.org/10.1111/j.1749-6632.1989.tb16477.x.

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5

Brunier, D., B. Michel, and S. D. Ehrlich. "Copy choice illegitimate DNA recombination." Cell 52, no. 6 (March 1988): 883–92. http://dx.doi.org/10.1016/0092-8674(88)90430-8.

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6

Onda, Masaaki, Junko Yamaguchi, Katsuhiro Hanada, Yasuo Asami, and Hideo Ikeda. "Role of DNA Ligase in the Illegitimate Recombination That Generates λbio-Transducing Phages in Escherichia coli." Genetics 158, no. 1 (May 1, 2001): 29–39. http://dx.doi.org/10.1093/genetics/158.1.29.

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Abstract We studied the role of DNA ligase in illegitimate recombination in Escherichia coli. A temperature-sensitive mutation in the lig gene reduced the frequency with which λbio-transducing phages were generated to 10-14% of that of wild type under UV irradiation. Reintroduction of the lig gene into this mutant restored the frequency of recombinant phage generation to that of wild type. Furthermore, overexpression of DNA ligase enhanced illegitimate recombination by 10-fold with or without UV irradiation. In addition, when DNA ligase was present in only limited amounts, UV-induced or spontaneous illegitimate recombination occurred exclusively at hotspot sites that have relatively long sequences of homology (9 or 13 bp). However, when DNA ligase was overexpressed, most of the illegitimate recombination took place at non-hotspot sites having only short sequences of homology (<4 bp). Thus, the level of ligase activity affects the frequency of illegitimate recombination, the length of sequence homology at the recombination sites, and the preference for recombination at hotspots, at least after UV irradiation. These observations support our hypothesis that the illegitimate recombination that generates λbio-transducing phages is mediated by the DNA break-and-join mechanism.

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7

Hanada, Katsuhiro, Teruhito Yamashita, Yuko Shobuike, and Hideo Ikeda. "Role of DnaB Helicase in UV-Induced Illegitimate Recombination in Escherichia coli." Journal of Bacteriology 183, no. 17 (September 1, 2001): 4964–69. http://dx.doi.org/10.1128/jb.183.17.4964-4969.2001.

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ABSTRACT To study the involvement of DNA replication in UV-induced illegitimate recombination, we examined the effect of temperature-sensitive dnaB mutations on illegitimate recombination and found that the frequency of illegitimate recombination was reduced by an elongation-deficient mutation,dnaB14, but not by an initiation-deficient mutation,dnaB252. This result indicates that DNA replication is required for UV-induced illegitimate recombination. In addition, thednaB14 mutation also affected spontaneous or UV-induced illegitimate recombination enhanced by the recQmutation. Nucleotide sequence analyses of the recombination junctions showed that DnaB-mediated illegitimate recombination is short homology dependent. Previously, Michel et al. (B. Michel, S. Ehrlich, and M. Uzest, EMBO J. 16:430–438, 1997) showed that thermal treatment of the temperature-sensitive dnaB8 mutant induces double-stranded breaks, implying that induction of illegitimate recombination occurs. To explain the discrepancy between the observations, we propose a model for DnaB function, in which thednaB mutations may exhibit two types of responses, early and late responses, for double-stranded break formation. In the early response, replication forks stall at damaged DNA, resulting in the formation of double-stranded breaks, and the dnaB14mutation reduces the double-stranded breaks shortly after temperature shift-up. On the other hand, in the late response, the arrested replication forks mediated by the dnaB8 mutation may induce double-stranded breaks after prolonged incubation.

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8

Sargent, R. G., M. A. Brenneman, and J. H. Wilson. "Repair of site-specific double-strand breaks in a mammalian chromosome by homologous and illegitimate recombination." Molecular and Cellular Biology 17, no. 1 (January 1997): 267–77. http://dx.doi.org/10.1128/mcb.17.1.267.

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In mammalian cells, chromosomal double-strand breaks are efficiently repaired, yet little is known about the relative contributions of homologous recombination and illegitimate recombination in the repair process. In this study, we used a loss-of-function assay to assess the repair of double-strand breaks by homologous and illegitimate recombination. We have used a hamster cell line engineered by gene targeting to contain a tandem duplication of the native adenine phosphoribosyltransferase (APRT) gene with an I-SceI recognition site in the otherwise wild-type APRT+ copy of the gene. Site-specific double-strand breaks were induced by intracellular expression of I-SceI, a rare-cutting endonuclease from the yeast Saccharomyces cerevisiae. I-SceI cleavage stimulated homologous recombination about 100-fold; however, illegitimate recombination was stimulated more than 1,000-fold. These results suggest that illegitimate recombination is an important competing pathway with homologous recombination for chromosomal double-strand break repair in mammalian cells.

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9

Onda, Masaaki, Katsuhiro Hanada, Hirokazu Kawachi, and Hideo Ikeda. "Escherichia coli MutM Suppresses Illegitimate Recombination Induced by Oxidative Stress." Genetics 151, no. 2 (February 1, 1999): 439–46. http://dx.doi.org/10.1093/genetics/151.2.439.

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Abstract DNA damage by oxidative stress is one of the causes of mutagenesis. However, whether or not DNA damage induces illegitimate recombination has not been determined. To study the effect of oxidative stress on illegitimate recombination, we examined the frequency of λbio transducing phage in the presence of hydrogen peroxide and found that this reagent enhances illegitimate recombination. To clarify the types of illegitimate recombination, we examined the effect of mutations in mutM and related genes on the process. The frequency of λbio transducing phage was 5- to 12-fold higher in the mutM mutant than in the wild type, while the frequency in the mutY and mutT mutants was comparable to that of the wild type. Because 7,8-dihydro-8-oxoguanine (8-oxoG) and formamido pyrimidine (Fapy) lesions can be removed from DNA by MutM protein, these lesions are thought to induce illegitimate recombination. Analysis of recombination junctions showed that the recombination at Hotspot I accounts for 22 or 4% of total λbio transducing phages in the wild type or in the mutM mutant, respectively. The preferential increase of recombination at nonhotspot sites with hydrogen peroxide in the mutM mutant was discussed on the basis of a new model, in which 8-oxoG and/or Fapy residues may introduce double-strand breaks into DNA.

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10

d'Alençon, E., M. Petranovic, B. Michel, P. Noirot, A. Aucouturier, M. Uzest, and S. D. Ehrlich. "Copy-choice illegitimate DNA recombination revisited." EMBO Journal 13, no. 11 (June 1994): 2725–34. http://dx.doi.org/10.1002/j.1460-2075.1994.tb06563.x.

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11

Ehrlich, S. D., and B. Michel. "Retraction: Copy choice illegitimate DNA recombination." Cell 62, no. 3 (August 1990): 409. http://dx.doi.org/10.1016/0092-8674(90)90004-x.

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12

Bashkirov, Vladimir I., Margarita M. Stoilova-Disheva, and Alexander A. Prozorov. "Interplasmidic illegitimate recombination in Bacillus subtilis." Molecular and General Genetics MGG 213, no. 2-3 (August 1988): 465–70. http://dx.doi.org/10.1007/bf00339617.

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13

Henderson, G., and J. P. Simons. "Processing of DNA prior to illegitimate recombination in mouse cells." Molecular and Cellular Biology 17, no. 7 (July 1997): 3779–85. http://dx.doi.org/10.1128/mcb.17.7.3779.

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In mammalian cells, the predominant pathway of chromosomal integration of exogenous DNA is random or illegitimate recombination; integration by homologous recombination is infrequent. Homologous recombination is initiated at double-strand DNA breaks which have been acted on by single-strand exonuclease. To further characterize the relationship between illegitimate and homologous recombination, we have investigated whether illegitimate recombination is also preceded by exonuclease digestion. Heteroduplex DNAs which included strand-specific restriction markers at each of four positions were generated. These DNAs were introduced into mouse embryonic stem cells, and stably transformed clones were isolated and analyzed to determine whether there was any strand bias in the retention of restriction markers with respect to their positions. Some of the mismatches appear to have been resolved by mismatch repair. Very significant strand bias was observed in the retention of restriction markers, and there was polarity of marker retention between adjacent positions. We conclude that DNA is frequently subjected to 5'-->3' exonuclease digestion prior to integration by illegitimate recombination and that the length of DNA removed by exonuclease digestion can be extensive. We also provide evidence which suggests that frequent but less extensive 3'-->5' exonuclease processing also occurs.

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14

Morris, Peter, Laura J. Marinelli, Deborah Jacobs-Sera, Roger W. Hendrix, and Graham F. Hatfull. "Genomic Characterization of Mycobacteriophage Giles: Evidence for Phage Acquisition of Host DNA by Illegitimate Recombination." Journal of Bacteriology 190, no. 6 (January 4, 2008): 2172–82. http://dx.doi.org/10.1128/jb.01657-07.

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ABSTRACT A characteristic feature of bacteriophage genomes is that they are architecturally mosaic, with each individual genome representing a unique assemblage of individual exchangeable modules. Plausible mechanisms for generating mosaicism include homologous recombination at shared boundary sequences of module junctions, illegitimate recombination in a non-sequence-directed process, and site-specific recombination. Analysis of the novel mycobacteriophage Giles genome not only extends our current perspective on bacteriophage genetic diversity, with more than 60% of the genes unrelated to other mycobacteriophages, but offers novel insights into how mosaic genomes are created. In one example, the integration/excision cassette is atypically situated within the structural gene operon and could have moved there either by illegitimate recombination or more plausibly via integrase-mediated site-specific recombination. In a second example, a DNA segment has been recently acquired from the host bacterial chromosome by illegitimate recombination, providing further evidence that phage genomic mosaicism is generated by nontargeted recombination processes.

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15

Cormack, Brendan P., and Stanley Falkow. "Efficient Homologous and Illegitimate Recombination in the Opportunistic Yeast Pathogen Candida glabrata." Genetics 151, no. 3 (March 1, 1999): 979–87. http://dx.doi.org/10.1093/genetics/151.3.979.

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Abstract The opportunistic pathogen Candida glabrata causes significant disease in humans. To develop genetic tools to investigate the pathogenicity of this organism, we have constructed ura3 and his3 auxotrophic strains by deleting the relevant coding regions in a C. glabrata clinical isolate. Linearized plasmids carrying a Saccharomyces cerevisiae URA3 gene efficiently transformed the ura3 auxotroph to prototrophy. Homologous recombination events were observed when the linearized plasmid carried short terminal regions homologous with the chromosome. In contrast, in the absence of any chromosomal homology, the plasmid integrated by illegitimate recombination into random sites in the genome. Sequence analysis of the target sites revealed that for the majority of illegitimate transformants there was no microhomology with the integration site. Approximately 0.25% of the insertions resulted in amino acid auxotrophy, suggesting that insertion was random at a gross level. Sequence analysis suggested that illegitimate recombination is nonrandom at the single-gene level and that the integrating plasmid has a preference for inserting into noncoding regions of the genome. Analysis of the relative numbers of homologous and illegitimate recombination events suggests that C. glabrata possesses efficient systems for both homologous and nonhomologous recombination.

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16

Kalpana, G. V., B. R. Bloom, and W. R. Jacobs. "Insertional mutagenesis and illegitimate recombination in mycobacteria." Proceedings of the National Academy of Sciences 88, no. 12 (June 15, 1991): 5433–37. http://dx.doi.org/10.1073/pnas.88.12.5433.

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17

Kantidze, Omar L., and Sergey V. Razin. "Chromatin loops, illegitimate recombination, and genome evolution." BioEssays 31, no. 3 (March 2009): 278–86. http://dx.doi.org/10.1002/bies.200800165.

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18

Zhu, J., and R. H. Schiestl. "Topoisomerase I involvement in illegitimate recombination in Saccharomyces cerevisiae." Molecular and Cellular Biology 16, no. 4 (April 1996): 1805–12. http://dx.doi.org/10.1128/mcb.16.4.1805.

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Chromosome aberrations may cause cancer and many heritable diseases. Topoisomerase I has been suspected of causing chromosome aberrations by mediating illegitimate recombination. The effects of deletion and of overexpression of the topoisomerase I gene on illegitimate recombination in the yeast Saccharomyces cerevisiae have been studied. Yeast transformations were carried out with DNA fragments that did not have any homology to the genomic DNA. The frequency of illegitimate integration was 6- to 12-fold increased in a strain overexpressing topoisomerase I compared with that in isogenic control strains. Hot spot sequences [(G/C)(A/T)T] for illegitimate integration target sites accounted for the majority of the additional events after overexpression of topoisomerase I. These hot spot sequences correspond to sequences previously identified in vitro as topoisomerase I preferred cleavage sequences in other organisms. Furthermore, such hot spot sequences were found in 44% of the integration events present in the TOP1 wild-type strain and at a significantly lower frequency in the top1delta strain. Our results provide in vivo evidence that a general eukaryotic topoisomerase I enzyme nicks DNA and ligates nonhomologous ends, leading to illegitimate recombination.

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19

Lehman, C. W., M. Clemens, D. K. Worthylake, J. K. Trautman, and D. Carroll. "Homologous and illegitimate recombination in developing Xenopus oocytes and eggs." Molecular and Cellular Biology 13, no. 11 (November 1993): 6897–906. http://dx.doi.org/10.1128/mcb.13.11.6897.

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Exogenous DNA is efficiently recombined when injected into the nuclei of Xenopus laevis oocytes. This reaction proceeds by a homologous resection-annealing mechanism which depends on the activity of a 5'-->3' exonuclease. Two possible functions for this recombination activity have been proposed: it may be a remnant of an early process in oogenesis, such as meiotic recombination or amplification of genes coding for rRNA, or it may reflect materials stored for embryogenesis. To test these hypotheses, recombination capabilities were examined with oocytes at various developmental stages. Late-stage oocytes performed only homologous recombination, whereas the smallest oocytes ligated the restriction ends of the injected DNA but supported no homologous recombination. This transition from ligation to recombination activity was also seen in nuclear extracts from these same stages. Exonuclease activity was measured in the nuclear extracts and found to be low in early stages and then to increase in parallel with recombination capacity in later stages. The accumulation of exonuclease and recombination activities during oogenesis suggests that they are stored for embryogenesis and are not present for oocyte-specific functions. Eggs were also tested and found to catalyze homologous recombination, ligation, and illegitimate recombination. Retention of homologous recombination in eggs is consistent with an embryonic function for the resection-annealing mechanism. The observation of all three reactions in eggs suggests that multiple pathways are available for the repair of double-strand breaks during the extremely rapid cleavage stages after fertilization.

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20

Lehman, C. W., M. Clemens, D. K. Worthylake, J. K. Trautman, and D. Carroll. "Homologous and illegitimate recombination in developing Xenopus oocytes and eggs." Molecular and Cellular Biology 13, no. 11 (November 1993): 6897–906. http://dx.doi.org/10.1128/mcb.13.11.6897-6906.1993.

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Exogenous DNA is efficiently recombined when injected into the nuclei of Xenopus laevis oocytes. This reaction proceeds by a homologous resection-annealing mechanism which depends on the activity of a 5'-->3' exonuclease. Two possible functions for this recombination activity have been proposed: it may be a remnant of an early process in oogenesis, such as meiotic recombination or amplification of genes coding for rRNA, or it may reflect materials stored for embryogenesis. To test these hypotheses, recombination capabilities were examined with oocytes at various developmental stages. Late-stage oocytes performed only homologous recombination, whereas the smallest oocytes ligated the restriction ends of the injected DNA but supported no homologous recombination. This transition from ligation to recombination activity was also seen in nuclear extracts from these same stages. Exonuclease activity was measured in the nuclear extracts and found to be low in early stages and then to increase in parallel with recombination capacity in later stages. The accumulation of exonuclease and recombination activities during oogenesis suggests that they are stored for embryogenesis and are not present for oocyte-specific functions. Eggs were also tested and found to catalyze homologous recombination, ligation, and illegitimate recombination. Retention of homologous recombination in eggs is consistent with an embryonic function for the resection-annealing mechanism. The observation of all three reactions in eggs suggests that multiple pathways are available for the repair of double-strand breaks during the extremely rapid cleavage stages after fertilization.

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21

Tsukamoto, Yasumasa, Jun-ichi Kato, and Hideo Ikeda. "Effects of Mutations of RAD50, RAD51, RAD52, and Related Genes on Illegitimate Recombination in Saccharomyces cerevisiae." Genetics 142, no. 2 (February 1, 1996): 383–91. http://dx.doi.org/10.1093/genetics/142.2.383.

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Abstract To examine the mechanism of illegitimate recombination in Saccharomyces cerevisiae, we have developed a plasmid system for quantitative analysis of deletion formation. A can1 cyh2 cell carrying two negative selection markers, the CAN1 and CYH2 genes, on a YCp plasmid is sensitive to canavanine and cycloheximide, but the cell becomes resistant to both drugs when the plasmid has a deletion over the CAN1 and CYH2 genes. Structural analysis of the recombinant plasmids obtained from the resistant cells showed that the plasmids had deletions at various sites of the CAN1-CYH2 region and there were only short regions of homology (1-5 bp) at the recombination junctions. The results indicated that the deletion detected in this system were formed by illegitimate recombination. Study on the effect of several rad mutations showed that the recombination rate was reduced by 30-, 10-, 10-, and 10-fold in the rad52, rad50, mre11, and xrs2 mutants, respectively, while in the rud51, 54, 55, and 57 mutants, the rate was comparable to that in the wild-type strain. The rad52 mutation did not affect length of homology at junction sites of illegitimate recombination.

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22

Lehman, Chris W., Jonathan K. Trautman, and Dana Carroll. "Illegitimate recombination inXenopus: characterization of end-joined junctions." Nucleic Acids Research 22, no. 3 (1994): 434–42. http://dx.doi.org/10.1093/nar/22.3.434.

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23

Ikeda, H. "Illegitimate recombination: Role of type II DNA topoisomerase." Advances in Biophysics 21 (1986): 149–60. http://dx.doi.org/10.1016/0065-227x(86)90020-1.

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24

Yarom, Rachel, Aviva Lapidot, Ada Neer, Nava Baran, and Haim Manor. "‘Illegitimate’ recombination events in polyoma-transformed rat cells." Gene 59, no. 1 (January 1987): 87–98. http://dx.doi.org/10.1016/0378-1119(87)90269-1.

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25

Allgood, N. D., and T. J. Silhavy. "Escherichia coli xonA (sbcB) mutants enhance illegitimate recombination." Genetics 127, no. 4 (April 1, 1991): 671–80. http://dx.doi.org/10.1093/genetics/127.4.671.

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Abstract Mutations of Escherichia coli K-12 were isolated that increase the frequency of deletion formation. Three of these mutations map to the gene sbcB at 43.5 min on the E. coli chromosome. Two types of mutations at sbcB have been previously defined: sbcB-type that suppress both the UV sensitivity and recombination deficiency of recBC mutants, and xonA-type that suppress only the UV sensitivity. Both types are defective for production of exonuclease I activity. The mutations isolated here were similar to xonA alleles of sbcB because they suppressed the UV sensitivity of recBC mutants but did not restore recombination proficiency. Indeed, two previously characterized xonA alleles were shown to increase the frequency of deletion formation, although an sbcB allele did not. This result demonstrates that loss of exonuclease I activity is not sufficient to confer a high deletion phenotype, rather, the product of the sbcB gene possesses some other function that is important for deletion formation. Because deletion formation in this system is recA independent and does not require extensive DNA homology, these mutations affect a pathway of illegitimate recombination.

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26

Harami, Gábor M., Yeonee Seol, Junghoon In, Veronika Ferencziová, Máté Martina, Máté Gyimesi, Kata Sarlós, et al. "Shuttling along DNA and directed processing of D-loops by RecQ helicase support quality control of homologous recombination." Proceedings of the National Academy of Sciences 114, no. 4 (January 9, 2017): E466—E475. http://dx.doi.org/10.1073/pnas.1615439114.

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Cells must continuously repair inevitable DNA damage while avoiding the deleterious consequences of imprecise repair. Distinction between legitimate and illegitimate repair processes is thought to be achieved in part through differential recognition and processing of specific noncanonical DNA structures, although the mechanistic basis of discrimination remains poorly defined. Here, we show thatEscherichia coliRecQ, a central DNA recombination and repair enzyme, exhibits differential processing of DNA substrates based on their geometry and structure. Through single-molecule and ensemble biophysical experiments, we elucidate how the conserved domain architecture of RecQ supports geometry-dependent shuttling and directed processing of recombination-intermediate [displacement loop (D-loop)] substrates. Our study shows that these activities together suppress illegitimate recombination in vivo, whereas unregulated duplex unwinding is detrimental for recombination precision. Based on these results, we propose a mechanism through which RecQ helicases achieve recombination precision and efficiency.

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27

Honma, M., L. S. Zhang, M. Hayashi, K. Takeshita, Y. Nakagawa, N. Tanaka, and T. Sofuni. "Illegitimate recombination leading to allelic loss and unbalanced translocation in p53-mutated human lymphoblastoid cells." Molecular and Cellular Biology 17, no. 8 (August 1997): 4774–81. http://dx.doi.org/10.1128/mcb.17.8.4774.

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Allelic loss and translocation are critical mutational events in human tumorigenesis. Allelic loss, which is usually identified as loss of heterozygosity (LOH), is frequently observed at tumor suppressor loci in various kinds of human tumors. It is generally thought to result from deletion or mitotic recombination between homologous chromosomes. In this report, we demonstrate that illegitimate (nonhomologous) recombination strongly contributes to the generation of allelic loss in p53-mutated cells. Spontaneous and X-ray-induced LOH mutations at the heterozygous thymidine kinase (tk) gene, which is located on the long arm of chromosome 17, from normal (TK6) and p53-mutated (WTK-1) human lymphoblastoid cells were cytogenetically analyzed by chromosome 17 painting. We observed unbalanced translocations in 53% of LOH mutants spontaneously arising from WTK-1 cells but none spontaneously arising from TK6 cells. We postulate that illegitimate recombination was occurring between nonhomologous chromosomes after DNA replication, leading to allelic loss and unbalanced translocations in p53-mutated WTK-1 cells. X-ray irradiation, which induces DNA double-strand breaks (DSBs), enhanced the generation of unbalanced translocation more efficiently in WTK-1 than in TK6 cells. This observation implicates the wild-type p53 protein in the regulation of homologous recombination and recombinational DNA repair of DSBs and suggests a possible mechanism by which loss of p53 function may cause genomic instability.

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28

Meima, R., B. J. Haijema, H. Dijkstra, G. J. Haan, G. Venema, and S. Bron. "Role of enzymes of homologous recombination in illegitimate plasmid recombination in Bacillus subtilis." Journal of bacteriology 179, no. 4 (1997): 1219–29. http://dx.doi.org/10.1128/jb.179.4.1219-1229.1997.

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29

Zucman-Rossi, J., P. Legoix, J. M. Victor, B. Lopez, and G. Thomas. "Chromosome translocation based on illegitimate recombination in human tumors." Proceedings of the National Academy of Sciences 95, no. 20 (September 29, 1998): 11786–91. http://dx.doi.org/10.1073/pnas.95.20.11786.

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30

Ikeda, H. "Bacteriophage T4 DNA topoisomerase mediates illegitimate recombination in vitro." Proceedings of the National Academy of Sciences 83, no. 4 (February 1, 1986): 922–26. http://dx.doi.org/10.1073/pnas.83.4.922.

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31

Chua, G. "Insertional mutagenesis based on illegitimate recombination in Schizosaccharomyces pombe." Nucleic Acids Research 28, no. 11 (June 1, 2000): 53e—53. http://dx.doi.org/10.1093/nar/28.11.e53.

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32

Michel, B., and S. D. Ehrlich. "Illegitimate recombination at the replication origin of bacteriophage M13." Proceedings of the National Academy of Sciences 83, no. 10 (May 1, 1986): 3386–90. http://dx.doi.org/10.1073/pnas.83.10.3386.

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33

Yang, W., and J. Summers. "Illegitimate replication of linear hepadnavirus DNA through nonhomologous recombination." Journal of virology 69, no. 7 (1995): 4029–36. http://dx.doi.org/10.1128/jvi.69.7.4029-4036.1995.

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34

Ikeda, Hideo. "Illegitimate recombination mediated by T4 DNA topoisomerase in vitro." Molecular and General Genetics MGG 202, no. 3 (March 1986): 518–20. http://dx.doi.org/10.1007/bf00333287.

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35

Shimizu, Hatsushi, Hirotaka Yamaguchi, Yuki Ashizawa, Yuko Kohno, Mihoko Asami, Jun-ichi Kato, and Hideo Ikeda. "Short-homology-independent illegitimate recombination in Escherichia coli : distinct mechanism from short-homology-dependent illegitimate recombination 1 1Edited by J. H. Miller." Journal of Molecular Biology 266, no. 2 (February 1997): 297–305. http://dx.doi.org/10.1006/jmbi.1996.0794.

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36

Lenz, Georg, Inga Nagel, Reiner Siebert, Anna V. Roschke, Warren Sanger, George W. Wright, Sandeep S. Dave, et al. "Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell–like diffuse large B cell lymphoma." Journal of Experimental Medicine 204, no. 3 (March 12, 2007): 633–43. http://dx.doi.org/10.1084/jem.20062041.

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To elucidate the mechanisms underlying chromosomal translocations in diffuse large B cell lymphoma (DLBCL), we investigated the nature and extent of immunoglobulin class switch recombination (CSR) in these tumors. We used Southern blotting to detect legitimate and illegitimate CSR events in tumor samples of the activated B cell–like (ABC), germinal center B cell–like (GCB), and primary mediastinal B cell lymphoma (PMBL) subgroups of DLBCL. The frequency of legitimate CSR was lower in ABC DLBCL than in GCB DLBCL and PMBL. In contrast, ABC DLBCL had a higher frequency of internal deletions within the switch μ (Sμ) region compared with GCB DLBCL and PMBL. ABC DLBCLs also had frequent deletions within Sγ and other illegitimate switch recombinations. Sequence analysis revealed ongoing Sμ deletions within ABC DLBCL tumor clones, which were accompanied by ongoing duplications and activation-induced cytidine deaminase–dependent somatic mutations. Unexpectedly, short fragments derived from multiple chromosomes were interspersed within Sμ in one case. These findings suggest that ABC DLBCLs have abnormalities in the regulation of CSR that could predispose to chromosomal translocations. Accordingly, aberrant switch recombination was responsible for translocations in ABC DLBCLs involving BCL6, MYC, and a novel translocation partner, SPIB.

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Harms, Klaus, Asbjørn Lunnan, Nils Hülter, Tobias Mourier, Lasse Vinner, Cheryl P. Andam, Pekka Marttinen, et al. "Substitutions of short heterologous DNA segments of intragenomic or extragenomic origins produce clustered genomic polymorphisms." Proceedings of the National Academy of Sciences 113, no. 52 (December 12, 2016): 15066–71. http://dx.doi.org/10.1073/pnas.1615819114.

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In a screen for unexplained mutation events we identified a previously unrecognized mechanism generating clustered DNA polymorphisms such as microindels and cumulative SNPs. The mechanism, short-patch double illegitimate recombination (SPDIR), facilitates short single-stranded DNA molecules to invade and replace genomic DNA through two joint illegitimate recombination events. SPDIR is controlled by key components of the cellular genome maintenance machinery in the gram-negative bacteriumAcinetobacter baylyi.The source DNA is primarily intragenomic but can also be acquired through horizontal gene transfer. The DNA replacements are nonreciprocal and locus independent. Bioinformatic approaches reveal occurrence of SPDIR events in the gram-positive human pathogenStreptococcus pneumoniaeand in the human genome.

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38

Shimizu, H., H. Yamaguchi, and H. Ikeda. "Molecular analysis of lambda bio transducing phage produced by oxolinic acid-induced illegitimate recombination in vivo." Genetics 140, no. 3 (July 1, 1995): 889–96. http://dx.doi.org/10.1093/genetics/140.3.889.

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Abstract To study the mechanism of DNA gyrase-mediated illegitimate recombination in Escherichia coli, we examined the formation of lambda Spi- phage during prophage induction. The frequency of Spi- phage was two to three orders of magnitude higher in the presence of oxolinic acid, an inhibitor of DNA gyrase A subunit, than in the absence of the drug, while it was very low in nalAr bacteria with the drug. RecA function is not required for the formation of these phages, indicating that this enhancement is not caused by the expression of SOS-controlled genes. Analyses of att region and recombination junctions of Spi- phages revealed that they have essentially the same structures as lambda bio transducing phages but are classified into two groups with respect to recombination sites. In the majority class of the transducing phages, there were not more than 3-bp homologies between the parental E. coli bio and lambda recombination sites. In the minority class of the transducing phages, on the other hand, 9-10-bp homologies were found between the parental recombination sites. These results suggested that oxolinic acid-induced illegitimate recombination takes place by two variants of a DNA gyrase-dependent mechanism.

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Semionov, Alexandre, Denis Cournoyer, and Terry Y. K. Chow. "1,5-isoquinolinediol increases the frequency of gene targeting by homologous recombination in mouse fibroblasts." Biochemistry and Cell Biology 81, no. 1 (January 1, 2003): 17–24. http://dx.doi.org/10.1139/o02-172.

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Gene targeting is a technique that allows the introduction of predefined alterations into chromosomal DNA. It involves a homologous recombination reaction between the targeted genomic sequence and an exogenous targeting vector. In theory, gene targeting constitutes the ideal method of gene therapy for single gene disorders. In practice, gene targeting remains extremely inefficient for at least two reasons: very low frequency of homologous recombination in mammalian cells and high proficiency of the mammalian cells to randomly integrate the targeting vector by illegitimate recombination. One known method to improve the efficiency of gene targeting is inhibition of poly(ADP-ribose)polymerase (PARP). It has been shown that PARP inhibitors, such as 3-methoxybenzamide, could lower illegitimate recombination, thus increasing the ratio of gene targeting to random integration. However, the above inhibitors were reported to decrease the absolute frequency of gene targeting. Here we show that treatment of mouse Ltk cells with 1,5-isoquinolinediol, a recent generation PARP inhibitor, leads to an increase up to 8-fold in the absolute frequency of gene targeting in the correction of the mutation at the stable integrated HSV tk gene.Key words: DNA recombination, gene targeting, PARP inhibition.

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40

Kusano, Kohji, Yasuo Asami, Ayumi Fujita, Masaru Tanokura, and Ichizo Kobayashi. "Type I restriction enzyme with RecA protein promotes illegitimate recombination." Plasmid 50, no. 3 (November 2003): 202–12. http://dx.doi.org/10.1016/j.plasmid.2003.07.001.

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41

Gheysen, G., R. Villarroel, and M. Van Montagu. "Illegitimate recombination in plants: a model for T-DNA integration." Genes & Development 5, no. 2 (February 1, 1991): 287–97. http://dx.doi.org/10.1101/gad.5.2.287.

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Schiestl, R. H., and T. D. Petes. "Integration of DNA fragments by illegitimate recombination in Saccharomyces cerevisiae." Proceedings of the National Academy of Sciences 88, no. 17 (September 1, 1991): 7585–89. http://dx.doi.org/10.1073/pnas.88.17.7585.

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Mayerhofer, R., Z. Koncz-Kalman, C. Nawrath, G. Bakkeren, A. Crameri, K. Angelis, G. P. Redei, J. Schell, B. Hohn, and C. Koncz. "T-DNA integration: a mode of illegitimate recombination in plants." EMBO Journal 10, no. 3 (March 1991): 697–704. http://dx.doi.org/10.1002/j.1460-2075.1991.tb07999.x.

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Shuman, S. "Vaccinia DNA topoisomerase I promotes illegitimate recombination in Escherichia coli." Proceedings of the National Academy of Sciences 86, no. 10 (May 1, 1989): 3489–93. http://dx.doi.org/10.1073/pnas.86.10.3489.

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Kegel, A. "Genome wide distribution of illegitimate recombination events in Kluyveromyces lactis." Nucleic Acids Research 34, no. 5 (March 6, 2006): 1633–45. http://dx.doi.org/10.1093/nar/gkl064.

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46

Chan, Cecilia Y., Jie Zhu, and Robert H. Schiestl. "Effect of rad50 mutation on illegitimate recombination in Saccharomyces cerevisiae." Molecular Genetics and Genomics 285, no. 6 (April 22, 2011): 471–84. http://dx.doi.org/10.1007/s00438-011-0619-y.

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47

Kehrenberg, Corinna, Nga Thi Thu Tham, and Stefan Schwarz. "New Plasmid-Borne Antibiotic Resistance Gene Cluster in Pasteurella multocida." Antimicrobial Agents and Chemotherapy 47, no. 9 (September 2003): 2978–80. http://dx.doi.org/10.1128/aac.47.9.2978-2980.2003.

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ABSTRACT A new antibiotic resistance gene cluster comprising genes for sulfonamide (sul2), streptomycin (strA-strB), and tetracycline [tetR-tet(H)] resistance was detected on plasmid pVM111 from Pasteurella multocida. The tetR-tet(H) gene region was inserted between sul2 and strA, possibly by illegitimate recombination. Two potential recombination sites of 18 and 25 bp were identified.

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Williams, T. J., and M. Fried. "Inverted duplication-transposition event in mammalian cells at an illegitimate recombination join." Molecular and Cellular Biology 6, no. 6 (June 1986): 2179–84. http://dx.doi.org/10.1128/mcb.6.6.2179.

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Illegitimate recombination events in mammalian cells often contain extraneous nucleotides or filler DNA at the recombinant joins. The polyomavirus-transformed cell line 7axB has previously been found to contain 37 base pairs (bp) of filler DNA at one virus-host join of the single insert of integrated viral DNA (A. Hayday, H. E. Ruley, and M. Fried, J. Virol. 44:67-77, 1982). By using a synthetic oligomer of these 37 bp as a probe, we demonstrated that this filler DNA is an inverted duplication of a single-copy rat sequence found 650 bp upstream from this virus-host join. The other virus-host join appears to be the result of a simple illegitimate recombination event between viral and host sequences. This is the first identification of filler DNA as a transposed copy of a chromosomal sequence. The relevance of the recombination events studied to cellular rearrangements and viral integration is discussed.

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49

Williams, T. J., and M. Fried. "Inverted duplication-transposition event in mammalian cells at an illegitimate recombination join." Molecular and Cellular Biology 6, no. 6 (June 1986): 2179–84. http://dx.doi.org/10.1128/mcb.6.6.2179-2184.1986.

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Illegitimate recombination events in mammalian cells often contain extraneous nucleotides or filler DNA at the recombinant joins. The polyomavirus-transformed cell line 7axB has previously been found to contain 37 base pairs (bp) of filler DNA at one virus-host join of the single insert of integrated viral DNA (A. Hayday, H. E. Ruley, and M. Fried, J. Virol. 44:67-77, 1982). By using a synthetic oligomer of these 37 bp as a probe, we demonstrated that this filler DNA is an inverted duplication of a single-copy rat sequence found 650 bp upstream from this virus-host join. The other virus-host join appears to be the result of a simple illegitimate recombination event between viral and host sequences. This is the first identification of filler DNA as a transposed copy of a chromosomal sequence. The relevance of the recombination events studied to cellular rearrangements and viral integration is discussed.

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50

Ho, P. Joy, Ross D. Brown, Gregory J. Pelka, Antony Basten, John Gibson, and Douglas E. Joshua. "Illegitimate switch recombinations are present in approximately half of primary myeloma tumors, but do not relate to known prognostic indicators or survival." Blood 97, no. 2 (January 15, 2001): 490–95. http://dx.doi.org/10.1182/blood.v97.2.490.

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Abstract The myeloma plasma cell is a postgerminal center, isotype-switched B cell. Chromosomal translocations into immunoglobulin heavy chain (IgH) switch regions, recombination sites in isotype switching, were initially demonstrated in myeloma cell lines but only a limited number of primary tumors. Molecular cytogenetics have since been applied to a series of primary tumors, in which IgH translocations accounted for many recurrent aberrations, among numerous nonrecurrent changes of unknown significance. This study, therefore, examined primary myeloma for IgH switch translocations using an established Southern blot assay that detected illegitimate switch recombinations. Sensitivity of the method was established by confining the analysis to 21 samples (4 stable, 17 progressive disease) with demonstrable legitimate isotype switches, of a total of 60 samples. Illegitimate recombinations were found in 12 or 57% (1 stable, 11 progressive) of 21 samples, comparable with estimates by molecular cytogenetics. The presence of switch translocations was supported by demonstrating up-regulated expression in myeloma marrow of cyclin D1 and fibroblast growth factor receptor 3 (FGFR3), candidate oncogenes on chromosomes 11q13 and 4p16, respectively. Illegitimate switches were detected most frequently in Sμ, with more than one region involved in 6 cases. Although these results confirmed the presence of switch translocations in primary myeloma, their absence in 43% of cases may imply heterogeneity of pathogenesis. In progressive disease, there was no significant difference between patients with and without illegitimate switches in survival, nor the prognostic indicators of β2microglobulin (β2m) and serum thymidine kinase (STK). Hence IgH switch translocations as a single entity are unlikely to be a feature of disease progression or have prognostic significance.

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