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Journal articles on the topic 'Homologous recombination repair'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Nowosielska, Anetta. "Bacterial DNA repair genes and their eukaryotic homologues: 5. The role of recombination in DNA repair and genome stability." Acta Biochimica Polonica 54, no. 3 (2007): 483–94. http://dx.doi.org/10.18388/abp.2007_3223.

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Recombinational repair is a well conserved DNA repair mechanism present in all living organisms. Repair by homologous recombination is generally accurate as it uses undamaged homologous DNA molecule as a repair template. In Escherichia coli homologous recombination repairs both the double-strand breaks and single-strand gaps in DNA. DNA double-strand breaks (DSB) can be induced upon exposure to exogenous sources such as ionizing radiation or endogenous DNA-damaging agents including reactive oxygen species (ROS) as well as during natural biological processes like conjugation. However, the bulk

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2

Kuzminov, Andrei. "Recombinational Repair of DNA Damage inEscherichia coli and Bacteriophage λ". Microbiology and Molecular Biology Reviews 63, № 4 (1999): 751–813. http://dx.doi.org/10.1128/mmbr.63.4.751-813.1999.

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SUMMARY Although homologous recombination and DNA repair phenomena in bacteria were initially extensively studied without regard to any relationship between the two, it is now appreciated that DNA repair and homologous recombination are related through DNA replication. In Escherichia coli, two-strand DNA damage, generated mostly during replication on a template DNA containing one-strand damage, is repaired by recombination with a homologous intact duplex, usually the sister chromosome. The two major types of two-strand DNA lesions are channeled into two distinct pathways of recombinational rep

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3

Kadyk, L. C., and L. H. Hartwell. "Sister chromatids are preferred over homologs as substrates for recombinational repair in Saccharomyces cerevisiae." Genetics 132, no. 2 (1992): 387–402. http://dx.doi.org/10.1093/genetics/132.2.387.

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Abstract A diploid Saccharomyces cerevisiae strain was constructed in which the products of both homolog recombination and unequal sister chromatid recombination events could be selected. This strain was synchronized in G1 or in G2, irradiated with X-rays to induce DNA damage, and monitored for levels of recombination. Cells irradiated in G1 were found to repair recombinogenic damage primarily by homolog recombination, whereas those irradiated in G2 repaired such damage preferentially by sister chromatid recombination. We found, as have others, that G1 diploids were much more sensitive to the

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4

Tamburini, Beth A., and Jessica K. Tyler. "Localized Histone Acetylation and Deacetylation Triggered by the Homologous Recombination Pathway of Double-Strand DNA Repair." Molecular and Cellular Biology 25, no. 12 (2005): 4903–13. http://dx.doi.org/10.1128/mcb.25.12.4903-4913.2005.

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ABSTRACT Many recent studies have demonstrated recruitment of chromatin-modifying enzymes to double-strand breaks. Instead, we wanted to examine chromatin modifications during the repair of these double-strand breaks. We show that homologous recombination triggers the acetylation of N-terminal lysines on histones H3 and H4 flanking a double-strand break, followed by deacetylation of H3 and H4. Consistent with a requirement for acetylation and deacetylation during homologous recombination, Saccharomyces cerevisiae with substitutions of the acetylatable lysines of histone H4, deleted for the N-t

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5

Bolt, Edward L., and Thorsten Allers. "New enzymes, new mechanisms?: DNA repair by recombination in the Archaea." Biochemist 26, no. 3 (2004): 19–21. http://dx.doi.org/10.1042/bio02603019.

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DNA repair by homologous recombination is highly accurate, since it uses an intact DNA strand to guide repair of its damaged homologue. This article focuses on two key steps in recombination: unwinding of strands by repair helicases, and annealing of homologous strands by strand-exchange enzymes.

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6

Inbar, Ori, and Martin Kupiec. "Homology Search and Choice of Homologous Partner during Mitotic Recombination." Molecular and Cellular Biology 19, no. 6 (1999): 4134–42. http://dx.doi.org/10.1128/mcb.19.6.4134.

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ABSTRACT Homologous recombination is an important DNA repair mechanism in vegetative cells. During the repair of double-strand breaks, genetic information is transferred between the interacting DNA sequences (gene conversion). This event is often accompanied by a reciprocal exchange between the homologous molecules, resulting in crossing over. The repair of DNA damage by homologous recombination with repeated sequences dispersed throughout the genome might result in chromosomal aberrations or in the inactivation of genes. It is therefore important to understand how the suitable homologous part

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7

Uchida, Tetsuya, Mariko Miyawaki, and Haruyasu Kinashi. "Chromosomal Arm Replacement in Streptomyces griseus." Journal of Bacteriology 185, no. 3 (2003): 1120–24. http://dx.doi.org/10.1128/jb.185.3.1120-1124.2003.

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ABSTRACT UV irradiation of Streptomyces griseus 2247 yielded a new chromosomal deletion mutant, MM9. Restriction and sequencing analysis revealed that homologous recombination between two similar lipoprotein-like open reading frames, which are located 450 and 250 kb from the left and right ends, respectively, caused chromosomal arm replacement. As a result, new 450-kb terminal inverted repeats (TIRs) were formed in place of the original 24-kb TIRs. Frequent homologous recombinations in Streptomyces strains suggest that telomere deletions can usually be repaired by recombinational DNA repair fu

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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 (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-speci

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9

Sweigert, S. E., and D. Carroll. "Repair and recombination of X-irradiated plasmids in Xenopus laevis oocytes." Molecular and Cellular Biology 10, no. 11 (1990): 5849–56. http://dx.doi.org/10.1128/mcb.10.11.5849.

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Plasmid DNA substrates were X-irradiated and injected into the nuclei of Xenopus laevis oocytes. After incubation for 20 h, DNA was recovered from the oocytes and analyzed simultaneously for repair and for intermolecular homologous recombination by electrophoresis and bacterial transformation. Oocyte-mediated repair of DNA strand breaks was observed with both methods. Using a repair-deficient mutant Escherichia coli strain and its repair-proficient parent as hosts for the transformation assay, we also demonstrated that oocytes repaired oxidative-type DNA base damage induced by X-rays. X-irradi

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10

Sweigert, S. E., and D. Carroll. "Repair and recombination of X-irradiated plasmids in Xenopus laevis oocytes." Molecular and Cellular Biology 10, no. 11 (1990): 5849–56. http://dx.doi.org/10.1128/mcb.10.11.5849-5856.1990.

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Plasmid DNA substrates were X-irradiated and injected into the nuclei of Xenopus laevis oocytes. After incubation for 20 h, DNA was recovered from the oocytes and analyzed simultaneously for repair and for intermolecular homologous recombination by electrophoresis and bacterial transformation. Oocyte-mediated repair of DNA strand breaks was observed with both methods. Using a repair-deficient mutant Escherichia coli strain and its repair-proficient parent as hosts for the transformation assay, we also demonstrated that oocytes repaired oxidative-type DNA base damage induced by X-rays. X-irradi

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11

Branzei, Dana, and Barnabas Szakal. "DNA helicases in homologous recombination repair." Current Opinion in Genetics & Development 71 (December 2021): 27–33. http://dx.doi.org/10.1016/j.gde.2021.06.009.

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12

Symington, Lorraine S. "Role of RAD52 Epistasis Group Genes in Homologous Recombination and Double-Strand Break Repair." Microbiology and Molecular Biology Reviews 66, no. 4 (2002): 630–70. http://dx.doi.org/10.1128/mmbr.66.4.630-670.2002.

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SUMMARY The process of homologous recombination is a major DNA repair pathway that operates on DNA double-strand breaks, and possibly other kinds of DNA lesions, to promote error-free repair. Central to the process of homologous recombination are the RAD52 group genes (RAD50, RAD51, RAD52, RAD54, RDH54/TID1, RAD55, RAD57, RAD59, MRE11, and XRS2), most of which were identified by their requirement for the repair of ionizing-radiation-induced DNA damage in Saccharomyces cerevisiae. The Rad52 group proteins are highly conserved among eukaryotes, and Rad51, Mre11, and Rad50 are also conserved in p

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13

Elliott, Beth, and Maria Jasin. "Repair of Double-Strand Breaks by Homologous Recombination in Mismatch Repair-Defective Mammalian Cells." Molecular and Cellular Biology 21, no. 8 (2001): 2671–82. http://dx.doi.org/10.1128/mcb.21.8.2671-2682.2001.

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ABSTRACT Chromosomal double-strand breaks (DSBs) stimulate homologous recombination by several orders of magnitude in mammalian cells, including murine embryonic stem (ES) cells, but the efficiency of recombination decreases as the heterology between the repair substrates increases (B. Elliott, C. Richardson, J. Winderbaum, J. A. Nickoloff, and M. Jasin, Mol. Cell. Biol. 18:93–101, 1998). We have now examined homologous recombination in mismatch repair (MMR)-defective ES cells to investigate both the frequency of recombination and the outcome of events. Using cells with a targeted mutation in

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14

Datta, A., A. Adjiri, L. New, G. F. Crouse, and S. Jinks Robertson. "Mitotic crossovers between diverged sequences are regulated by mismatch repair proteins in Saccaromyces cerevisiae." Molecular and Cellular Biology 16, no. 3 (1996): 1085–93. http://dx.doi.org/10.1128/mcb.16.3.1085.

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Mismatch repair systems correct replication- and recombination-associated mispaired bases and influence the stability of simple repeats. These systems thus serve multiple roles in maintaining genetic stability in eukaryotes, and human mismatch repair defects have been associated with hereditary predisposition to cancer. In prokaryotes, mismatch repair systems also have been shown to limit recombination between diverged (homologous) sequences. We have developed a unique intron-based assay system to examine the effects of yeast mismatch repair genes (PMS1, MSH2, and MSH3) on crossovers between h

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15

Saleh-Gohari, Nasrollah, Helen E. Bryant, Niklas Schultz, Kayan M. Parker, Tobias N. Cassel, and Thomas Helleday. "Spontaneous Homologous Recombination Is Induced by Collapsed Replication Forks That Are Caused by Endogenous DNA Single-Strand Breaks." Molecular and Cellular Biology 25, no. 16 (2005): 7158–69. http://dx.doi.org/10.1128/mcb.25.16.7158-7169.2005.

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ABSTRACT Homologous recombination is vital to repair fatal DNA damage during DNA replication. However, very little is known about the substrates or repair pathways for homologous recombination in mammalian cells. Here, we have compared the recombination products produced spontaneously with those produced following induction of DNA double-strand breaks (DSBs) with the I-SceI restriction endonuclease or after stalling or collapsing replication forks following treatment with thymidine or camptothecin, respectively. We show that each lesion produces different spectra of recombinants, suggesting di

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16

Wang, Xin, Carolyn A. Peterson, Huyong Zheng, Rodney S. Nairn, Randy J. Legerski, and Lei Li. "Involvement of Nucleotide Excision Repair in a Recombination-Independent and Error-Prone Pathway of DNA Interstrand Cross-Link Repair." Molecular and Cellular Biology 21, no. 3 (2001): 713–20. http://dx.doi.org/10.1128/mcb.21.3.713-720.2001.

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ABSTRACT DNA interstrand cross-links (ICLs) block the strand separation necessary for essential DNA functions such as transcription and replication and, hence, represent an important class of DNA lesion. Since both strands of the double helix are affected in cross-linked DNA, it is likely that conservative recombination using undamaged homologous regions as a donor may be required to repair ICLs in an error-free manner. However, in Escherichia coli and yeast, recombination-independent mechanisms of ICL repair have been identified in addition to recombinational repair pathways. To study the rep

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17

Dang, Tuyen T., and Julio C. Morales. "XRN2 Links RNA:DNA Hybrid Resolution to Double Strand Break Repair Pathway Choice." Cancers 12, no. 7 (2020): 1821. http://dx.doi.org/10.3390/cancers12071821.

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It was recently shown that the 5’ to 3’ exoribonuclease XRN2 is involved in the DNA damage response. Importantly, loss of XRN2 abrogates DNA double stranded break repair via the non-homologous end-joining pathway. However, the mechanistic details of how XRN2 functions in the non-homologous end-joining repair process are unknown. In this study, we elucidated that XRN2-mediated RNA:DNA hybrid resolution is required to allow Ku70 binding to DNA ends. These data suggest that XRN2 is required for the initiation of non-homologous end-joining repair. Interestingly, we uncovered a role for XRN2 in the

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18

Huselid, Eric, and Samuel F. Bunting. "The Regulation of Homologous Recombination by Helicases." Genes 11, no. 5 (2020): 498. http://dx.doi.org/10.3390/genes11050498.

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Homologous recombination is essential for DNA repair, replication and the exchange of genetic material between parental chromosomes during meiosis. The stages of recombination involve complex reorganization of DNA structures, and the successful completion of these steps is dependent on the activities of multiple helicase enzymes. Helicases of many different families coordinate the processing of broken DNA ends, and the subsequent formation and disassembly of the recombination intermediates that are necessary for template-based DNA repair. Loss of recombination-associated helicase activities ca

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19

Rijkers, Tonnie, Jody Van Den Ouweland, Bruno Morolli, et al. "Targeted Inactivation of Mouse RAD52Reduces Homologous Recombination but Not Resistance to Ionizing Radiation." Molecular and Cellular Biology 18, no. 11 (1998): 6423–29. http://dx.doi.org/10.1128/mcb.18.11.6423.

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ABSTRACT The RAD52 epistasis group is required for recombinational repair of double-strand breaks (DSBs) and shows strong evolutionary conservation. In Saccharomyces cerevisiae, RAD52 is one of the key members in this pathway. Strains with mutations in this gene show strong hypersensitivity to DNA-damaging agents and defects in recombination. Inactivation of the mouse homologue of RAD52in embryonic stem (ES) cells resulted in a reduced frequency of homologous recombination. Unlike the yeast Scrad52 mutant,MmRAD52 −/− ES cells were not hypersensitive to agents that induce DSBs. MmRAD52 null mut

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20

Lin, Yunfu, Tamas Lukacsovich, and Alan S. Waldman. "Multiple Pathways for Repair of DNA Double-Strand Breaks in Mammalian Chromosomes." Molecular and Cellular Biology 19, no. 12 (1999): 8353–60. http://dx.doi.org/10.1128/mcb.19.12.8353.

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ABSTRACT To study repair of DNA double-strand breaks (DSBs) in mammalian chromosomes, we designed DNA substrates containing a thymidine kinase (TK) gene disrupted by the 18-bp recognition site for yeast endonuclease I-SceI. Some substrates also contained a second defective TK gene sequence to serve as a genetic donor in recombinational repair. A genomic DSB was induced by introducing endonuclease I-SceI into cells containing a stably integrated DNA substrate. DSB repair was monitored by selection for TK-positive segregants. We observed that intrachromosomal DSB repair is accomplished with near

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21

Sun, Yueru, Thomas J. McCorvie, Luke A. Yates, and Xiaodong Zhang. "Structural basis of homologous recombination." Cellular and Molecular Life Sciences 77, no. 1 (2019): 3–18. http://dx.doi.org/10.1007/s00018-019-03365-1.

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AbstractHomologous recombination (HR) is a pathway to faithfully repair DNA double-strand breaks (DSBs). At the core of this pathway is a DNA recombinase, which, as a nucleoprotein filament on ssDNA, pairs with homologous DNA as a template to repair the damaged site. In eukaryotes Rad51 is the recombinase capable of carrying out essential steps including strand invasion, homology search on the sister chromatid and strand exchange. Importantly, a tightly regulated process involving many protein factors has evolved to ensure proper localisation of this DNA repair machinery and its correct timing

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22

Johnson, R. D., and M. Jasin. "Double-strand-break-induced homologous recombination in mammalian cells." Biochemical Society Transactions 29, no. 2 (2001): 196–201. http://dx.doi.org/10.1042/bst0290196.

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In mammalian cells, the repair of DNA double-strand breaks (DSBs) occurs by both homologous and non-homologous mechanisms. Indirect evidence, including that from gene targeting and random integration experiments, had suggested that non-homologous mechanisms were significantly more frequent than homologous ones. However, more recent experiments indicate that homologous recombination is also a prominent DSB repair pathway. These experiments show that mammalian cells use homologous sequences located at multiple positions throughout the genome to repair a DSB. However, template preference appears

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23

Priebe, S. D., J. Westmoreland, T. Nilsson-Tillgren, and M. A. Resnick. "Induction of recombination between homologous and diverged DNAs by double-strand gaps and breaks and role of mismatch repair." Molecular and Cellular Biology 14, no. 7 (1994): 4802–14. http://dx.doi.org/10.1128/mcb.14.7.4802.

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Sequence homology is expected to influence recombination. To further understand mechanisms of recombination and the impact of reduced homology, we examined recombination during transformation between plasmid-borne DNA flanking a double-strand break (DSB) or gap and its chromosomal homolog. Previous reports have concentrated on spontaneous recombination or initiation by undefined lesions. Sequence divergence of approximately 16% reduced transformation frequencies by at least 10-fold. Gene conversion patterns associated with double-strand gap repair of episomal plasmids or with plasmid integrati

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Priebe, S. D., J. Westmoreland, T. Nilsson-Tillgren, and M. A. Resnick. "Induction of recombination between homologous and diverged DNAs by double-strand gaps and breaks and role of mismatch repair." Molecular and Cellular Biology 14, no. 7 (1994): 4802–14. http://dx.doi.org/10.1128/mcb.14.7.4802-4814.1994.

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Sequence homology is expected to influence recombination. To further understand mechanisms of recombination and the impact of reduced homology, we examined recombination during transformation between plasmid-borne DNA flanking a double-strand break (DSB) or gap and its chromosomal homolog. Previous reports have concentrated on spontaneous recombination or initiation by undefined lesions. Sequence divergence of approximately 16% reduced transformation frequencies by at least 10-fold. Gene conversion patterns associated with double-strand gap repair of episomal plasmids or with plasmid integrati

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25

Bärtsch, Stephan, Leslie E. Kang, and Lorraine S. Symington. "RAD51 Is Required for the Repair of Plasmid Double-Stranded DNA Gaps from Either Plasmid or Chromosomal Templates." Molecular and Cellular Biology 20, no. 4 (2000): 1194–205. http://dx.doi.org/10.1128/mcb.20.4.1194-1205.2000.

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ABSTRACT DNA double-strand breaks may be induced by endonucleases, ionizing radiation, chemical agents, and mechanical forces or by replication of single-stranded nicked chromosomes. Repair of double-strand breaks can occur by homologous recombination or by nonhomologous end joining. A system was developed to measure the efficiency of plasmid gap repair by homologous recombination using either chromosomal or plasmid templates. Gap repair was biased toward gene conversion events unassociated with crossing over using either donor sequence. The dependence of recombinational gap repair on genes be

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26

Evers, Bastiaan, Thomas Helleday, and Jos Jonkers. "Targeting homologous recombination repair defects in cancer." Trends in Pharmacological Sciences 31, no. 8 (2010): 372–80. http://dx.doi.org/10.1016/j.tips.2010.06.001.

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27

Jasin, M., and R. Rothstein. "Repair of Strand Breaks by Homologous Recombination." Cold Spring Harbor Perspectives in Biology 5, no. 11 (2013): a012740. http://dx.doi.org/10.1101/cshperspect.a012740.

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28

Spies, Maria, and Richard Fishel. "Mismatch Repair during Homologous and Homeologous Recombination." Cold Spring Harbor Perspectives in Biology 7, no. 3 (2015): a022657. http://dx.doi.org/10.1101/cshperspect.a022657.

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29

Wyman, Claire, Dejan Ristic, and Roland Kanaar. "Homologous recombination-mediated double-strand break repair." DNA Repair 3, no. 8-9 (2004): 827–33. http://dx.doi.org/10.1016/j.dnarep.2004.03.037.

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Yokochi, T., K. Kusano, and I. Kobayashi. "Evidence for conservative (two-progeny) DNA double-strand break repair." Genetics 139, no. 1 (1995): 5–17. http://dx.doi.org/10.1093/genetics/139.1.5.

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Abstract The double-strand break repair models for homologous recombination propose that a double-strand break in a duplex DNA segment is repaired by gene conversion copying a homologous DNA segment. This is a type of conservative recombination, or two-progeny recombination, which generates two duplex DNA segments from two duplex DNA segments. Transformation with a plasmid carrying a double-strand gap and an intact homologous DNA segment resulted in products expected from such conservative (two-progeny) repair in Escherichia coli cells with active E. coli RecE pathway (recBC sbcA) or with acti

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Ohba, Shigeo, Kei Yamashiro, and Yuichi Hirose. "Inhibition of DNA Repair in Combination with Temozolomide or Dianhydrogalactiol Overcomes Temozolomide-Resistant Glioma Cells." Cancers 13, no. 11 (2021): 2570. http://dx.doi.org/10.3390/cancers13112570.

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Resistance to temozolomide and intratumoral heterogeneity contribute to the poor prognosis of glioma. The mechanisms of temozolomide resistance can vary within a heterogeneous tumor. Temozolomide adds a methyl group to DNA. The primary cytotoxic lesion, O6-methylguanine, mispairs with thymine, leading to a futile DNA mismatch repair cycle, formation of double-strand breaks, and eventual cell death when O6-methylguanine DNA methyltransferase (MGMT) is absent. N7-methylguanine and N3-methyladenine are repaired by base excision repair (BER). The study aim was to elucidate temozolomide resistance

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32

Takata, Minoru, Masao S. Sasaki, Eiichiro Sonoda, et al. "The Rad51 Paralog Rad51B Promotes Homologous Recombinational Repair." Molecular and Cellular Biology 20, no. 17 (2000): 6476–82. http://dx.doi.org/10.1128/mcb.20.17.6476-6482.2000.

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ABSTRACT The highly conserved Saccharomyces cerevisiae Rad51 protein plays a central role in both mitotic and meiotic homologous DNA recombination. Seven members of the Rad51 family have been identified in vertebrate cells, including Rad51, Dmc1, and five Rad51-related proteins referred to as Rad51 paralogs, which share 20 to 30% sequence identity with Rad51. In chicken B lymphocyte DT40 cells, we generated a mutant with RAD51B/RAD51L1, a member of the Rad51 family, knocked out. RAD51B −/− cells are viable, although spontaneous chromosomal aberrations kill about 20% of the cells in each cell c

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Spek, Erik J., Laurel N. Vuong, Tetsuya Matsuguchi, Martin G. Marinus, and Bevin P. Engelward. "Nitric Oxide-Induced Homologous Recombination in Escherichia coli Is Promoted by DNA Glycosylases." Journal of Bacteriology 184, no. 13 (2002): 3501–7. http://dx.doi.org/10.1128/jb.184.13.3501-3507.2002.

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ABSTRACT Nitric oxide (NO.) is involved in neurotransmission, inflammation, and many other biological processes. Exposure of cells to NO. leads to DNA damage, including formation of deaminated and oxidized bases. Apurinic/apyrimidinic (AP) endonuclease-deficient cells are sensitive to NO. toxicity, which indicates that base excision repair (BER) intermediates are being generated. Here, we show that AP endonuclease-deficient cells can be protected from NO. toxicity by inactivation of the uracil (Ung) or formamidopyrimidine (Fpg) DNA glycosylases but not by inactivation of a 3-methyladenine (Alk

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Moldovan, George-Lucian, Mahesh V. Madhavan, Kanchan D. Mirchandani, Ryan M. McCaffrey, Patrizia Vinciguerra, and Alan D. D'Andrea. "DNA Polymerase POLN Participates in Cross-Link Repair and Homologous Recombination." Molecular and Cellular Biology 30, no. 4 (2009): 1088–96. http://dx.doi.org/10.1128/mcb.01124-09.

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ABSTRACT All cells rely on DNA polymerases to duplicate their genetic material and to repair or bypass DNA lesions. In humans, 16 polymerases have been identified, and each bears specific functions in genome maintenance. We identified here the recently discovered polymerase POLN to be involved in repair of DNA cross-links. Such DNA lesions are highly toxic and are believed to be repaired by the sequential activity of nucleotide excision repair, translesion synthesis, and homologous recombination mechanisms. By functionally assaying its role in these processes, we unraveled an unexpected involv

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35

Porter, Gregory, Jim Westmoreland, Scott Priebe, and Michael A. Resnick. "Homologous and Homeologous Intermolecular Gene Conversion Are Not Differentially Affected by Mutations in the DNA Damage or the Mismatch Repair Genes RAD1, RAD50, RAD51, RAD52, RAD54, PMS1 and MSH2." Genetics 143, no. 2 (1996): 755–67. http://dx.doi.org/10.1093/genetics/143.2.755.

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Abstract Mismatch repair (MMR) genes or genes involved in both DNA damage repair and homologous recombination might affect homeologous us. homologous recombination differentially. Spontaneous mitotic gene conversion between a chromosome and a homologous or homeologous donor sequence (14% diverged) on a single copy plasmid was examined in wild-type Saccharomyces cerevisiae strains and in MMR or DNA damage repair mutants. Homologous recombination in rad51, rad52 and rad54 mutants was considerably reduced, while there was little effect of radl, rad50, pms1 and msh2 null mutations. DNA divergence

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36

Bartl, Thomas, and Alex Farr. "Homologous recombination deficiency in breast cancer." memo - Magazine of European Medical Oncology 13, no. 4 (2020): 375–79. http://dx.doi.org/10.1007/s12254-020-00624-x.

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SummaryBRCA mutation-related DNA repair deficiencies increase the individual sensitivity to DNA-targeting agents. Therefore, the patient’s BRCA mutational status is evaluated in clinical practice as a predictive marker in response to platinum salts and poly-ADP-ribose polymerase (PARP) inhibitors for breast cancer treatment. A substantial subset of BRCA wild-type breast cancer lesions, however, share both prominent molecular characteristics and clinical behavior patterns with cancer that harbors BRCA mutations, including DNA repair deficiencies. Also referred to as “BRCAness”, this observation

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Siede, Wolfram, Anna A. Friedl, Irina Dianova, Friederike Eckardt-Schupp, and Errol C. Friedberg. "The Saccharomyces cerevisiae Ku Autoantigen Homologue Affects Radiosensitivity Only in the Absence of Homologous Recombination." Genetics 142, no. 1 (1996): 91–102. http://dx.doi.org/10.1093/genetics/142.1.91.

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In mammalian cells, all subunits of the DNA-dependent protein kinase (DNA-PK) have been implicated in the repair of DNA double-strand breaks and in V(D)J recombination. In the yeast Saccharomyces cerevisiae, we have examined the phenotype conferred by a deletion of HDF1, the putative homologue of the 70-kD subunit of the DNA-end binding Ku complex of DNA-PK. The yeast gene does not play a role in radiation-induced cell cycle checkpoint arrest in G1 and G2 or in hydroxyurea-induced checkpoint arrest in S. In cells competent for homologous recombination, we could not detect any sensitivity to io

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Borts, R. H., W. Y. Leung, W. Kramer, et al. "Mismatch repair-induced meiotic recombination requires the pms1 gene product." Genetics 124, no. 3 (1990): 573–84. http://dx.doi.org/10.1093/genetics/124.3.573.

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Abstract The presence of multiple heterologies in a 9-kilobase (kb) interval results in a decrease in meiotic crossovers from 26.0% to 10.1%. There is also an increase from 3.5% to 11.1% in gene conversions and ectopic recombinations between the flanking homologous MAT loci. The hypothesis that mismatch repair of heteroduplex DNA containing several heterologies would lead to a second round of recombination has now been tested by examining the effect of a mutation that reduces mismatch correction. The repair-defective pms1-1 allele restores the pattern of recombination to nearly that seen in co

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Ira, Grzegorz, and James E. Haber. "Characterization of RAD51-Independent Break-Induced Replication That Acts Preferentially with Short Homologous Sequences." Molecular and Cellular Biology 22, no. 18 (2002): 6384–92. http://dx.doi.org/10.1128/mcb.22.18.6384-6392.2002.

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ABSTRACT Repair of double-strand breaks by gene conversions between homologous sequences located on different Saccharomyces cerevisiae chromosomes or plasmids requires RAD51. When repair occurs between inverted repeats of the same plasmid, both RAD51-dependent and RAD51-independent repairs are found. Completion of RAD51-independent plasmid repair events requires RAD52, RAD50, RAD59, TID1 (RDH54), and SRS2 and appears to involve break-induced replication coupled to single-strand annealing. Surprisingly, RAD51-independent recombination requires much less homology (30 bp) for strand invasion than

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Saparbaev, Murat, Louise Prakash, and Satya Prakash. "Requirement of Mismatch Repair Genes MSH2 and MSH3 in the RAD1-RAD10 Pathway of Mitotic Recombination in Saccharomyces cerevisiae." Genetics 142, no. 3 (1996): 727–36. http://dx.doi.org/10.1093/genetics/142.3.727.

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Abstract The RAD1 and RAD10 genes of Saccharomyces cerevisiae are required for nucleotide excision repair and they also act in mitotic recombination. The Rad1-Rad10 complex has a single-stranded DNA endonuclease activity. Here, we show that the mismatch repair genes MSH2 and MSH3 function in mitotic recombination. For both his3 and his4 duplications, and for homologous integration of a linear DNA fragment into the genome, the msh3Δ mutation has an effect on recombination similar to that of the rad1Δ and rad10Δ mutations. The msh2Δ mutation also reduces the rate of recombination of the his3 dup

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Burton, Peter, David J. McBride, Jonathan M. Wilkes, J. David Barry, and Richard McCulloch. "Ku Heterodimer-Independent End Joining in Trypanosoma brucei Cell Extracts Relies upon Sequence Microhomology." Eukaryotic Cell 6, no. 10 (2007): 1773–81. http://dx.doi.org/10.1128/ec.00212-07.

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ABSTRACT DNA double-strand breaks (DSBs) are repaired primarily by two distinct pathways: homologous recombination and nonhomologous end joining (NHEJ). NHEJ has been found in all eukaryotes examined to date and has been described recently for some bacterial species, illustrating its ancestry. Trypanosoma brucei is a divergent eukaryotic protist that evades host immunity by antigenic variation, a process in which homologous recombination plays a crucial function. While homologous recombination has been examined in some detail in T. brucei, little work has been done to examine what other DSB re

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Coulon, Stéphane, Eishi Noguchi, Chiaki Noguchi, Li-Lin Du, Toru M. Nakamura, and Paul Russell. "Rad22Rad52-dependent Repair of Ribosomal DNA Repeats Cleaved by Slx1-Slx4 Endonuclease." Molecular Biology of the Cell 17, no. 4 (2006): 2081–90. http://dx.doi.org/10.1091/mbc.e05-11-1006.

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Slx1 and Slx4 are subunits of a structure-specific DNA endonuclease that is found in Saccharomyces cerevisiae, Schizosaccharomyces pombe, and other eukaryotic species. It is thought to initiate recombination events or process recombination structures that occur during the replication of the tandem repeats of the ribosomal DNA (rDNA) locus. Here, we present evidence that fission yeast Slx1-Slx4 initiates homologous recombination events in the rDNA repeats that are processed by a mechanism that requires Rad22 (Rad52 homologue) but not Rhp51 (Rad51 homologue). Slx1 is required to generate ∼50% of

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Vijayan, Poornima, and Luisa Bonilla. "A brief overview of homologous recombination deficiency testing in cancers for the ‘Next-Generation’ Pathologist." Journal of Pathology of Nepal 10, no. 2 (2020): 1760–65. http://dx.doi.org/10.3126/jpn.v10i2.29862.

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Genomic instability is one of the hallmarks of cancer, having a crucial role in cancer pathogenesis as well as tumor proliferation. This essential feature is secondary to dysregulation of DNA damage repair pathways. Homologous repair represents the most reliable double-strand break repair mechanism. Homologous recombination deficiency is responsible for generating and perpetuating DNA damage in cancer, posing an opportunity for targeting treatment with poly(ADP-ribose) polymerase inhibitors through ‘synthetic lethality’, as well as platinum-based agents. Comprehensive genomic analysis has made

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Elliott, Beth, Christine Richardson, Jamie Winderbaum, Jac A. Nickoloff, and Maria Jasin. "Gene Conversion Tracts from Double-Strand Break Repair in Mammalian Cells." Molecular and Cellular Biology 18, no. 1 (1998): 93–101. http://dx.doi.org/10.1128/mcb.18.1.93.

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ABSTRACT Mammalian cells are able to repair chromosomal double-strand breaks (DSBs) both by homologous recombination and by mechanisms that require little or no homology. Although spontaneous homologous recombination is rare, DSBs will stimulate recombination by 2 to 3 orders of magnitude when homology is provided either from exogenous DNA in gene-targeting experiments or from a repeated chromosomal sequence. Using a gene-targeting assay in mouse embryonic stem cells, we now investigate the effect of heterology on recombinational repair of DSBs. Cells were cotransfected with an endonuclease ex

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Kline, Kimberly A., and H. Steven Seifert. "Role of the Rep Helicase Gene in Homologous Recombination in Neisseria gonorrhoeae." Journal of Bacteriology 187, no. 8 (2005): 2903–7. http://dx.doi.org/10.1128/jb.187.8.2903-2907.2005.

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ABSTRACT In Escherichia coli, the Rep helicase has been implicated in replication fork progression, replication restart, homologous recombination, and DNA repair. We show that a Neisseria gonorrhoeae rep mutant is deficient in the homologous-recombination-mediated processes of DNA transformation and pilus-based colony variation but not in DNA repair.

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Latypov, Vitaly, Maja Rothenberg, Alexander Lorenz, et al. "Roles of Hop1 and Mek1 in Meiotic Chromosome Pairing and Recombination Partner Choice in Schizosaccharomyces pombe." Molecular and Cellular Biology 30, no. 7 (2010): 1570–81. http://dx.doi.org/10.1128/mcb.00919-09.

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ABSTRACT Synaptonemal complex (SC) proteins Hop1 and Mek1 have been proposed to promote homologous recombination in meiosis of Saccharomyces cerevisiae by establishment of a barrier against sister chromatid recombination. Therefore, it is interesting to know whether the homologous proteins play a similar role in Schizosaccharomyces pombe. Unequal sister chromatid recombination (USCR) was found to be increased in hop1 and mek1 single and double deletion mutants in assays for intrachromosomal recombination (ICR). Meiotic intergenic (crossover) and intragenic (conversion) recombination between ho

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Wagener-Ryczek, Svenja, Sabine Merkelbach-Bruse, and Janna Siemanowski. "Biomarkers for Homologous Recombination Deficiency in Cancer." Journal of Personalized Medicine 11, no. 7 (2021): 612. http://dx.doi.org/10.3390/jpm11070612.

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DNA double-strand breaks foster tumorigenesis and cell death. Two distinct mechanisms can be activated by the cell for DNA repair: the accurate mechanism of homologous recombination repair or the error-prone non-homologous end joining. Homologous Recombination Deficiency (HRD) is associated with sensitivity towards PARP inhibitors (PARPi) and its determination is used as a biomarker for therapy decision making. Nevertheless, the biology of HRD is rather complex and the application, as well as the benefit of the different HRD biomarker assays, is controversial. Acquiring knowledge of the underl

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Bressan, Debra A., Bonnie K. Baxter, and John H. J. Petrini. "The Mre11-Rad50-Xrs2 Protein Complex Facilitates Homologous Recombination-Based Double-Strand Break Repair inSaccharomyces cerevisiae." Molecular and Cellular Biology 19, no. 11 (1999): 7681–87. http://dx.doi.org/10.1128/mcb.19.11.7681.

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ABSTRACT Saccharomyces cerevisiae mre11Δ mutants are profoundly deficient in double-strand break (DSB) repair, indicating that the Mre11-Rad50-Xrs2 protein complex plays a central role in the cellular response to DNA DSBs. In this study, we examined the role of the complex in homologous recombination, the primary mode of DSB repair in yeast. We measured survival in synchronous cultures following irradiation and scored sister chromatid and interhomologue recombination genetically. mre11Δ strains were profoundly sensitive to ionizing radiation (IR) throughout the cell cycle. Mutant strains exhib

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Sharma, Shilpy, J. Kevin Hicks, Colleen L. Chute та ін. "REV1 and polymerase ζ facilitate homologous recombination repair". Nucleic Acids Research 40, № 2 (2011): 682–91. http://dx.doi.org/10.1093/nar/gkr769.

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Dudáš, Andrej, and Miroslav Chovanec. "DNA double-strand break repair by homologous recombination." Mutation Research/Reviews in Mutation Research 566, no. 2 (2004): 131–67. http://dx.doi.org/10.1016/j.mrrev.2003.07.001.

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