Relevant bibliographies by topics / Illegitimate recombination

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Academic literature on the topic 'Illegitimate recombination'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Illegitimate recombination"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Illegitimate recombination"

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Pinder, David. "Illegitimate recombination in plasmids." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/11260.

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Illegitimate recombination mechanisms are important for genetic change within an organism. They are also the cause of many instability problems in biotechnology and have been associated with certain human genetic disorders and cancers. The original aim of this work was to construct a deletion (illegitimate recombination) resistant cosmid based, cloning system, for the cloning of unstable human DNA. Two 'mutant plasmids' pMS5 and pMS7 were isolated. The plasmids were derived from pUC18 and appeared to stabilise the propagation of a long DNA palindrome. The basic concept was to construct a new cosmid using pMS7 as part of the backbone. The construction of two new cosmids cDRII (Deletion Resistant) and cDRIII is described. However, they are unlikely to contain a mutation which stabilises unstable sequences. This thesis also describes the search for the 'mutation' in pMS7 by, single-strand conformation polymorphism and fragment swap analysis. This work led to the isolation of a novel mutation composed of both direct and inverted repeats, which I have called DIR. The presence of DIR in pAC2 (a derivative of pUC18, with the same DNA palindrome as pMS7), supports the absence of a stabilising 'mutation in pMS7. The structure of the DIR mutation is analysed in detail and a hypothesis for its formation is proposed. Finally, the behaviour of four long DNA palindromes (other than that cloned in pMS7), is investigated when ligated into pM* (a derivative of pMS7).
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Blake, Catherine E. "Illegitimate recombination in Escherichia coli." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/15058.

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The factors affecting deletion of long DNA palindromes from high copy number cloning vectors are investigated with particular reference to the mode of deletion and it is shown that the deletion of a 571 bp palindrome deleted from pMS7 using 3 bp repeats. A shorter 109 bp palindrome deleted from a related plasmid using 7 bp direct repeats and the mode of deletion is unaffected by the genotype of the host strain. There also appears to be a bias for the deletion of palindromic sequences on the lagging strand of a replication fork. It is also shown that in a wild-type E. coli strain there is inhibition of plasmid multimerization if the plasmids carry long palindromic sequences. It is proposed that the lack of plasmid multimers in this background is a result of the removal of palindromic sequences form the plasmids by the SbcCD protein of E. coli. In an sbcCD strain, plasmid DNA bearing long palindromes is not detected in a monomeric form, instead the DNA is present in multimeric forms, predominantly dimers. The ability to form plasmid multimers in this background may help to stabilise the palindromic sequences. The behaviour of palindromic sequences carried on plasmids is also investigated in recA sbcCD strains with a view to the correct choice of E. coli strain for the cloning of long palindromic sequences. Finally, the influence of an sbcCD mutation on the formation of araB-lacZ cistron fusion is investigated. The SbcCd proteins are thought to have a role in the processing of secondary structures formed by palindromic sequences. The formation of araB-lacZ fusions occurs via a strand transfer complex involving a complex genome rearrangement and secondary structure. Although an sbcCD mutation did not affect the kinetics or sequences specificity of fusion formation it is possible that SbcCD might have a role in processing the strand transfer complex which is not easily detected.
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Bush, Natassja. "The role of DNA gyrase in illegitimate recombination." Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/66586/.

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DNA, due to its double-helical structure, is subject to changes in topology due to the nature of transcription and replication. To overcome this, cells have processes and enzymes that ameliorate these changes. One such group of enzymes are the DNA topoisomerases, which are responsible for the maintenance of DNA topology. Despite this important role, these enzymes participate in illegitimate recombination (IR), which is genetic recombination between regions of DNA that share little or no homology. This can result in chromosomal rearrangements and is often a consequence of DNA-damaging agents. A consequence of topoisomerase-induced IR is thought to be therapy-related acute myeloid leukaemia (tAML). Analogously, there is evidence that exposure to sublethal concentrations of ciprofloxacin, a topoisomerase inhibitor, can cause resistance to non-quinolone antibiotics. This may work by a similar mechanism as that proposed for t-AML. This project centres around the examination of DNA gyrase-mediated IR focussing on the proposed subunit-exchange model. Using Blue-Native PAGE, I set up an assay to examine subunit exchange in topoisomerases. I have also characterised previously identified gyrase hyper-recombination mutations, known to increase the frequency of IR. Furthermore, I have investigated quinolone-induced antibiotic resistance and what the mechanism is. Here, I show that DNA gyrase can undergo subunit exchange, and that this seems to occur within higherorder oligomers of the enzyme, which have not been investigated before. Biochemical characterisation of the hyper-recombination mutations shows that they impair DNA gyrase activity which, in vivo, may have downstream consequences that may lead to IR. Using an in vivo assay where E. coli is treated with subinhibitory levels of quinolones, I have seen resistance to other non-quinolone antibiotics. This is not seen when other antibiotics, including other topoisomerase inhibitors, are tested. Whole genome sequencing has revealed point mutations that explain the resistances seen, however other larger chromosomal modifications have been observed as well.
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Hinds, Jason. "The molecular genetics of homologous and illegitimate recombination in mycobacteria." Thesis, London School of Hygiene and Tropical Medicine (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298244.

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Kyryk, Anzhela. "DSB repair by illegitimate and homologous DNA recombination in Arabidopsis thaliana." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=96435859X.

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Higashi, Atsuko. "Direct Hematological Toxicity and Illegitimate Chromosomal Recombination Caused by the Systemic Activation of CreERT2." Kyoto University, 2010. http://hdl.handle.net/2433/97950.

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Chan, Cecilia Yuen-Ting. "The studies of double strand break-induced microhomology-mediated illegitimate recombination and its genetic control." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1581660331&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Michel, Bénédicte. "Recombinaison homologue et illegitime chez bacillus subtilis et escherichia coli." Paris 6, 1986. http://www.theses.fr/1986PA066534.

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Kyryk, Anzhela [Verfasser]. "DSB repair by illegitimate and homologous DNA recombination in Arabidopsis thaliana / von Anzhela Kyryk." 2001. http://d-nb.info/96435859X/34.

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Book chapters on the topic "Illegitimate recombination"

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Michel, Bénédicte. "Illegitimate Recombination in Bacteria." In Organization of the Prokaryotic Genome, 129–50. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818180.ch8.

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Auzanneau, Céline, and Philippe Pourquier. "DNA Topoisomerase I and Illegitimate Recombination." In Cancer Drug Discovery and Development, 119–43. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0323-4_6.

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Wilson, Thomas E. "Nonhomologous end-joining: mechanisms, conservation and relationship to illegitimate recombination." In Molecular Genetics of Recombination, 487–513. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71021-9_17.

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van Rijk, Anke, and Hans Bloemendal. "Molecular mechanisms of exon shuffling: illegitimate recombination." In Contemporary Issues in Genetics and Evolution, 245–49. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-010-0229-5_13.

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Hill, Stuart A., Sandra G. Morrison, and John Swanson. "Illegitimate Recombination and Gonococcal Pilin Gene Variation." In Neisseriae 1990, edited by Mark Achtman, Peter Kohl, Christian Marchal, Giovanna Morelli, Andrea Seiler, and Burghard Thiesen, 425–30. Berlin, Boston: De Gruyter, 1991. http://dx.doi.org/10.1515/9783110867787-075.

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Pinta, V., M. Picaud, and C. Astier. "Molecular Characterization of Illegitimate Recombination in Rubrivivax Gelatinosus." In Photosynthesis: Mechanisms and Effects, 2885–88. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-3953-3_676.

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Müller, J. R., S. Janz, and M. Potter. "Illegitimate Recombinations Between c-myc and Immunoglobulin Loci are Remodeled by Deletions in Mouse Plasmacytomas but not in Burkitt’s Lymphomas." In Current Topics in Microbiology and Immunology, 425–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_49.

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Carroll, D. "Illegitimate Recombination." In Encyclopedia of Genetics, 996–98. Elsevier, 2001. http://dx.doi.org/10.1006/rwgn.2001.0666.

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Carroll, D. "Illegitimate Recombination." In Brenner's Encyclopedia of Genetics, 18. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-374984-0.00768-3.

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"Illegitimate Recombination." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 960. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8274.

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Reports on the topic "Illegitimate recombination"

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Grant, Stephen G. Increased Illegitimate V(D)J Recombination as a Possible Marker for Breast Cancer Predisposition. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada423210.

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