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Journal articles on the topic 'Replicative recombination'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Weerasooriya, Savithri, Katherine A. DiScipio, Anthar S. Darwish, Ping Bai, and Sandra K. Weller. "Herpes simplex virus 1 ICP8 mutant lacking annealing activity is deficient for viral DNA replication." Proceedings of the National Academy of Sciences 116, no. 3 (2018): 1033–42. http://dx.doi.org/10.1073/pnas.1817642116.

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Most DNA viruses that use recombination-dependent mechanisms to replicate their DNA encode a single-strand annealing protein (SSAP). The herpes simplex virus (HSV) single-strand DNA binding protein (SSB), ICP8, is the central player in all stages of DNA replication. ICP8 is a classical replicative SSB and interacts physically and/or functionally with the other viral replication proteins. Additionally, ICP8 can promote efficient annealing of complementary ssDNA and is thus considered to be a member of the SSAP family. The role of annealing during HSV infection has been difficult to assess in pa

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2

Gallei, Andreas, Alexander Pankraz, Heinz-Jürgen Thiel, and Paul Becher. "RNA Recombination In Vivo in the Absence of Viral Replication." Journal of Virology 78, no. 12 (2004): 6271–81. http://dx.doi.org/10.1128/jvi.78.12.6271-6281.2004.

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ABSTRACT To study fundamental aspects of RNA recombination, an in vivo RNA recombination system was established. This system allowed the efficient generation of recombinant cytopathogenic pestiviruses after transfection of synthetic, nonreplicatable, subgenomic transcripts in cells infected with a replicating noncytopathogenic virus. Studies addressing the interplay between RNA recombination and replication revealed that cotransfection of noninfected cells with various pairs of nonreplicatable RNA derivatives also led to the emergence of recombinant viral genomes. Remarkably, homologous and no

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3

Yonesaki, T. "Involvement of a replicative DNA helicase of bacteriophage T4 in DNA recombination." Genetics 138, no. 2 (1994): 247–52. http://dx.doi.org/10.1093/genetics/138.2.247.

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Abstract Bacteriophage T4 gene 41 encodes a replicative DNA helicase that is a subunit of the primosome which is essential for lagging-strand DNA synthesis. A mutation, rrh, was generated and selected in the helicase gene on the basis of limited DNA replication that ceases early. The survival of ultraviolet-irradiated phage and the frequency of genetic recombination are reduced by rrh. In addition, rrh diminishes the production of concatemeric DNA. These results strongly suggest that the gene 41 replicative helicase participates in DNA recombination.

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4

Hayashi, Yasuyuki, Yoshiyuki Kitamura, Mayumi Nakanishi, and Katsuro Koike. "The Binding Site of Transcription Factor YY1 Is Required for Intramolecular Recombination between Terminally Repeated Sequences of Linear Replicative Hepatitis B Virus DNA." Journal of Virology 74, no. 20 (2000): 9471–78. http://dx.doi.org/10.1128/jvi.74.20.9471-9478.2000.

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ABSTRACT In the replication cycle of hepadnavirus DNA, the double-stranded linear form of viral DNA is generated as a minor replicative intermediate, which is efficiently converted to covalently closed circular DNA (cccDNA) by intramolecular recombination (W. Yang and J. Summers, J. Virol. 69:4029–4036, 1995). We previously found a binding site of transcription factor Yin and Yang 1 (YY1) in one terminal region of the double-stranded linear replicative hepatitis B virus (HBV) DNA (M. Nakanishi-Matsui, Y. Hayashi, Y. Kitamura, and K. Koike, J. Virol. 74:5562–5568, 2000). However, it is not know

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Tsai, Yun-Luen, Shun-Fu Tseng, Shih-Husan Chang, Chuan-Chuan Lin, and Shu-Chun Teng. "Involvement of Replicative Polymerases, Tel1p, Mec1p, Cdc13p, and the Ku Complex in Telomere-Telomere Recombination." Molecular and Cellular Biology 22, no. 16 (2002): 5679–87. http://dx.doi.org/10.1128/mcb.22.16.5679-5687.2002.

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ABSTRACT Telomere maintenance is required for chromosome stability, and telomeres are typically replicated by the action of the reverse transcriptase telomerase. In both tumor and yeast cells that lack telomerase, telomeres are maintained by an alternative recombination mechanism. Genetic studies have led to the identification of DNA polymerases, cell cycle checkpoint proteins, and telomere binding proteins involved in the telomerase pathway. However, how these proteins affect telomere-telomere recombination has not been identified to date. Using an assay to trace the in vivo recombinational p

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6

Gómez-González, Belén, Irene Felipe-Abrio, and Andrés Aguilera. "The S-Phase Checkpoint Is Required To Respond to R-Loops Accumulated in THO Mutants." Molecular and Cellular Biology 29, no. 19 (2009): 5203–13. http://dx.doi.org/10.1128/mcb.00402-09.

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ABSTRACT Cotranscriptional R-loops are formed in yeast mutants of the THO complex, which functions at the interface between transcription and mRNA export. Despite the relevance of R-loops in transcription-associated recombination, the mechanisms by which they trigger recombination are still elusive. In order to understand how R-loops compromise genome stability, we have analyzed the genetic interaction of THO with 26 genes involved in replication, S-phase checkpoint, DNA repair, and chromatin remodeling. We found a synthetic growth defect in double null mutants of THO and S-phase checkpoint fa

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7

Dudas, Kathleen C., and Kenneth N. Kreuzer. "UvsW Protein Regulates Bacteriophage T4 Origin-Dependent Replication by Unwinding R-Loops." Molecular and Cellular Biology 21, no. 8 (2001): 2706–15. http://dx.doi.org/10.1128/mcb.21.8.2706-2715.2001.

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ABSTRACT The UvsW protein of bacteriophage T4 is involved in many aspects of phage DNA metabolism, including repair, recombination, and recombination-dependent replication. UvsW has also been implicated in the repression of origin-dependent replication at late times of infection, when UvsW is normally synthesized. Two well-characterized T4 origins, ori(uvsY) andori(34), are believed to initiate replication through an R-loop mechanism. Here we provide both in vivo and in vitro evidence that UvsW is an RNA-DNA helicase that catalyzes the dissociation of RNA from origin R-loops. Two-dimensional g

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8

Evans, David Hugh. "Poxvirus Recombination." Pathogens 11, no. 8 (2022): 896. http://dx.doi.org/10.3390/pathogens11080896.

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Genetic recombination is used as a tool for modifying the composition of poxvirus genomes in both discovery and applied research. This review documents the history behind the development of these tools as well as what has been learned about the processes that catalyze virus recombination and the links between it and DNA replication and repair. The study of poxvirus recombination extends back to the 1930s with the discovery that one virus can reactivate another by a process later shown to generate recombinants. In the years that followed it was shown that recombinants can be produced in virus-b

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9

Prado, Félix. "Homologous Recombination: To Fork and Beyond." Genes 9, no. 12 (2018): 603. http://dx.doi.org/10.3390/genes9120603.

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Accurate completion of genome duplication is threatened by multiple factors that hamper the advance and stability of the replication forks. Cells need to tolerate many of these blocking lesions to timely complete DNA replication, postponing their repair for later. This process of lesion bypass during DNA damage tolerance can lead to the accumulation of single-strand DNA (ssDNA) fragments behind the fork, which have to be filled in before chromosome segregation. Homologous recombination plays essential roles both at and behind the fork, through fork protection/lesion bypass and post-replicative

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10

Lehmann, Carl P., Alberto Jiménez-Martín, Dana Branzei, and José Antonio Tercero. "Prevention of unwanted recombination at damaged replication forks." Current Genetics 66, no. 6 (2020): 1045–51. http://dx.doi.org/10.1007/s00294-020-01095-7.

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Abstract Homologous recombination is essential for the maintenance of genome integrity but must be strictly controlled to avoid dangerous outcomes that produce the opposite effect, genomic instability. During unperturbed chromosome replication, recombination is globally inhibited at ongoing DNA replication forks, which helps to prevent deleterious genomic rearrangements. This inhibition is carried out by Srs2, a helicase that binds to SUMOylated PCNA and has an anti-recombinogenic function at replication forks. However, at damaged stalled forks, Srs2 is counteracted and DNA lesion bypass can b

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11

Shammas, Masood A., Shujuan J. Xia, and Robert J. Shmookler Reis. "Induction of Duplication Reversion in Human Fibroblasts, by Wild-Type and Mutated SV40 T Antigen, Covaries With the Ability to Induce Host DNA Synthesis." Genetics 146, no. 4 (1997): 1417–28. http://dx.doi.org/10.1093/genetics/146.4.1417.

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Intrachromosomal homologous recombination, manifest as reversion of a 14-kbp duplication in the hypoxanthine phosphoribosyl transferase (HPRT) gene, is elevated in human cells either stably transformed or transiently transfected by the SV40 (simian virus 40) large T antigen gene. Following introduction of wild-type SV40, or any of several T-antigen point mutations in a constant SV40 background, we observed a strong correlation between the stimulation of chromosomal recombination and induction of host-cell DNA synthesis. Moreover, inhibitors of DNA replication (aphidicolin and hydroxyurea) supp

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12

Popov, N. N., T. Yu. Kolotova, and M. B. Davidenko. "Mechanisms and regulation of rna virus recombination." Annals of Mechnikov Institute, no. 3 (October 1, 2017): 7–17. https://doi.org/10.5281/zenodo.1000128.

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This review attempts to summarize the most important data concerning of molecular mechanisms and regulation of the viral recombination. Two mechanisms are responsible for RNA virus recombination, specifically replicative recombination based on replicase template switching and nonreplicative joining among fragments of viral origin. Retroviruses recombination occurs during DNA synthesis, whereby reverse transcriptase undergoes template switching between the two copackaged RNAs, However numerous questions about molecular mechanisms of RNA recombination remain unanswered. RNA recombination is one

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13

Rogers, Colette B., Wendy Leung, Ryan M. Baxley, et al. "Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination." Biomolecules 15, no. 1 (2025): 150. https://doi.org/10.3390/biom15010150.

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RAD18 is a conserved eukaryotic E3 ubiquitin ligase that promotes genome stability through multiple pathways. One of these is gap-filling DNA synthesis at active replication forks and in post-replicative DNA. RAD18 also regulates homologous recombination (HR) repair of DNA breaks; however, the current literature describing the contribution of RAD18 to HR in mammalian systems has not reached a consensus. To investigate this, we examined three independent RAD18-null human cell lines. Our analyses found that loss of RAD18 in HCT116, but neither hTERT RPE-1 nor DLD1 cell lines, resulted in elevate

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14

Zaman, Shamsu, Malay Choudhury, James C. Jiang, et al. "Mechanism of Regulation of Intrachromatid Recombination and Long-Range Chromosome Interactions in Saccharomyces cerevisiae." Molecular and Cellular Biology 36, no. 10 (2016): 1451–63. http://dx.doi.org/10.1128/mcb.01100-15.

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The NAD-dependent histone deacetylase Sir2 controls ribosomal DNA (rDNA) silencing by inhibiting recombination and RNA polymerase II-catalyzed transcription in the rDNA ofSaccharomyces cerevisiae. Sir2 is recruited to nontranscribed spacer 1 (NTS1) of the rDNA array by interaction between the RENT (regulation ofnucleolarsilencing andtelophase exit) complex and the replication terminator protein Fob1. The latter binds to its cognate sites, called replication termini (Ter) or replication fork barriers (RFB), that are located in each copy of NTS1. This work provides new mechanistic insights into

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15

Hsieh, C. L., R. P. McCloskey, E. Radany, and M. R. Lieber. "V(D)J recombination: evidence that a replicative mechanism is not required." Molecular and Cellular Biology 11, no. 8 (1991): 3972–77. http://dx.doi.org/10.1128/mcb.11.8.3972-3977.1991.

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We examined a series of extrachromosomal DNA substrates for V(D)J recombination under replicating and nonreplicating conditions. Complete and partial replications were examined by monitoring the loss of prokaryote-specific adenine methylation at 14 to 22 MboI-DpnI restriction sites (GATC) on the substrates. Some of these sites are within 2 bases of the signal sequence ends. We found that neither coding joint nor signal joint formation requires substrate replication. After ruling out replication as a substrate requirement, we determined whether replication had any effect on the efficiency of V(

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Hsieh, C. L., R. P. McCloskey, E. Radany, and M. R. Lieber. "V(D)J recombination: evidence that a replicative mechanism is not required." Molecular and Cellular Biology 11, no. 8 (1991): 3972–77. http://dx.doi.org/10.1128/mcb.11.8.3972.

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We examined a series of extrachromosomal DNA substrates for V(D)J recombination under replicating and nonreplicating conditions. Complete and partial replications were examined by monitoring the loss of prokaryote-specific adenine methylation at 14 to 22 MboI-DpnI restriction sites (GATC) on the substrates. Some of these sites are within 2 bases of the signal sequence ends. We found that neither coding joint nor signal joint formation requires substrate replication. After ruling out replication as a substrate requirement, we determined whether replication had any effect on the efficiency of V(

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17

Lorenz, Alexander, Fekret Osman, Victoria Folkyte, Sevil Sofueva, and Matthew C. Whitby. "Fbh1 Limits Rad51-Dependent Recombination at Blocked Replication Forks." Molecular and Cellular Biology 29, no. 17 (2009): 4742–56. http://dx.doi.org/10.1128/mcb.00471-09.

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ABSTRACT Controlling the loading of Rad51 onto DNA is important for governing when and how homologous recombination is used. Here we use a combination of genetic assays and indirect immunofluorescence to show that the F-box DNA helicase (Fbh1) functions in direct opposition to the Rad52 orthologue Rad22 to curb Rad51 loading onto DNA in fission yeast. Surprisingly, this activity is unnecessary for limiting spontaneous direct-repeat recombination. Instead it appears to play an important role in preventing recombination when replication forks are blocked and/or broken. When overexpressed, Fbh1 s

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18

Öling, David, Rehan Masoom, and Kristian Kvint. "Loss of Ubp3 increases silencing, decreases unequal recombination in rDNA, and shortens the replicative life span in Saccharomyces cerevisiae." Molecular Biology of the Cell 25, no. 12 (2014): 1916–24. http://dx.doi.org/10.1091/mbc.e13-10-0591.

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Ubp3 is a conserved ubiquitin protease that acts as an antisilencing factor in MAT and telomeric regions. Here we show that ubp3∆ mutants also display increased silencing in ribosomal DNA (rDNA). Consistent with this, RNA polymerase II occupancy is lower in cells lacking Ubp3 than in wild-type cells in all heterochromatic regions. Moreover, in a ubp3∆ mutant, unequal recombination in rDNA is highly suppressed. We present genetic evidence that this effect on rDNA recombination, but not silencing, is entirely dependent on the silencing factor Sir2. Further, ubp3∆ sir2∆ mutants age prematurely at

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19

Dixon, L., T. Nyffenegger, G. Delley, J. Martinez-Izquierdo, and T. Hohn. "Evidence for replicative recombination in cauliflower mosaic virus." Virology 150, no. 2 (1986): 463–68. http://dx.doi.org/10.1016/0042-6822(86)90310-7.

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20

Gmyl, Anatoly P., Evgeny V. Belousov, Svetlana V. Maslova, Elena V. Khitrina, Alexander B. Chetverin, and Vadim I. Agol. "Nonreplicative RNA Recombination in Poliovirus." Journal of Virology 73, no. 11 (1999): 8958–65. http://dx.doi.org/10.1128/jvi.73.11.8958-8965.1999.

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ABSTRACT Current models of recombination between viral RNAs are based on replicative template-switch mechanisms. The existence of nonreplicative RNA recombination in poliovirus is demonstrated in the present study by the rescue of viable viruses after cotransfections with different pairs of genomic RNA fragments with suppressed translatable and replicating capacities. Approximately 100 distinct recombinant genomes have been identified. The majority of crossovers occurred between nonhomologous segments of the partners and might have resulted from transesterification reactions, not necessarily i

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Simon, Marie-Noëlle, Dmitri Churikov, and Vincent Géli. "Replication stress as a source of telomere recombination during replicative senescence inSaccharomyces cerevisiae." FEMS Yeast Research 16, no. 7 (2016): fow085. http://dx.doi.org/10.1093/femsyr/fow085.

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Alli, Nabilah, Anna Lou-Hing, Edward L. Bolt, and Liu He. "POLD3 as Controller of Replicative DNA Repair." International Journal of Molecular Sciences 25, no. 22 (2024): 12417. http://dx.doi.org/10.3390/ijms252212417.

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Multiple modes of DNA repair need DNA synthesis by DNA polymerase enzymes. The eukaryotic B-family DNA polymerase complexes delta (Polδ) and zeta (Polζ) help to repair DNA strand breaks when primed by homologous recombination or single-strand DNA annealing. DNA synthesis by Polδ and Polζ is mutagenic, but is needed for the survival of cells in the presence of DNA strand breaks. The POLD3 subunit of Polδ and Polζ is at the heart of DNA repair by recombination, by modulating polymerase functions and interacting with other DNA repair proteins. We provide the background to POLD3 discovery, investi

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Cromie, Gareth A., Catherine B. Millar, Kristina H. Schmidt, and David R. F. Leach. "Palindromes as Substrates for Multiple Pathways of Recombination in Escherichia coli." Genetics 154, no. 2 (2000): 513–22. http://dx.doi.org/10.1093/genetics/154.2.513.

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Abstract A 246-bp imperfect palindrome has the potential to form hairpin structures in single-stranded DNA during replication. Genetic evidence suggests that these structures are converted to double-strand breaks by the SbcCD nuclease and that the double-strand breaks are repaired by recombination. We investigated the role of a range of recombination mutations on the viability of cells containing this palindrome. The palindrome was introduced into the Escherichia coli chromosome by phage λ lysogenization. This was done in both wt and sbcC backgrounds. Repair of the SbcCD-induced double-strand

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Novarina, Daniele, Ridhdhi Desai, Jessica A. Vaisica, et al. "A Genome-Wide Screen for Genes Affecting Spontaneous Direct-Repeat Recombination in Saccharomyces cerevisiae." G3: Genes|Genomes|Genetics 10, no. 6 (2020): 1853–67. http://dx.doi.org/10.1534/g3.120.401137.

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Homologous recombination is an important mechanism for genome integrity maintenance, and several homologous recombination genes are mutated in various cancers and cancer-prone syndromes. However, since in some cases homologous recombination can lead to mutagenic outcomes, this pathway must be tightly regulated, and mitotic hyper-recombination is a hallmark of genomic instability. We performed two screens in Saccharomyces cerevisiae for genes that, when deleted, cause hyper-recombination between direct repeats. One was performed with the classical patch and replica-plating method. The other was

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Matsumoto, Seiji, and Hisao Masai. "Regulation of chromosome dynamics by Hsk1/Cdc7 kinase." Biochemical Society Transactions 41, no. 6 (2013): 1712–19. http://dx.doi.org/10.1042/bst20130217.

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Hsk1 (homologue of Cdc7 kinase 1) of the fission yeast is a member of the conserved Cdc7 (cell division cycle 7) kinase family, and promotes initiation of chromosome replication by phosphorylating Mcm (minichromosome maintenance) subunits, essential components for the replicative helicase. Recent studies, however, indicate more diverse roles for Hsk1/Cdc7 in regulation of various chromosome dynamics, including initiation of meiotic recombination, meiotic chromosome segregation, DNA repair, replication checkpoints, centromeric heterochromatin formation and so forth. Hsk1/Cdc7, with its unique t

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Rattray, Alison J., Brenda K. Shafer, Carolyn B. McGill, and Jeffrey N. Strathern. "The Roles of REV3 and RAD57 in Double-Strand-Break-Repair-Induced Mutagenesis of Saccharomyces cerevisiae." Genetics 162, no. 3 (2002): 1063–77. http://dx.doi.org/10.1093/genetics/162.3.1063.

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Abstract The DNA synthesis associated with recombinational repair of chromosomal double-strand breaks (DSBs) has a lower fidelity than normal replicative DNA synthesis. Here, we use an inverted-repeat substrate to monitor the fidelity of repair of a site-specific DSB. DSB induction made by the HO endonuclease stimulates recombination &gt;5000-fold and is associated with a &gt;1000-fold increase in mutagenesis of an adjacent gene. We demonstrate that most break-repair-induced mutations (BRIMs) are point mutations and have a higher proportion of frameshifts than do spontaneous mutations

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Wang, Xu-Shan, Benjawan Khuntirat, Keyun Qing, et al. "Characterization of Wild-Type Adeno-Associated Virus Type 2-Like Particles Generated during Recombinant Viral Vector Production and Strategies for Their Elimination." Journal of Virology 72, no. 7 (1998): 5472–80. http://dx.doi.org/10.1128/jvi.72.7.5472-5480.1998.

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ABSTRACT The pSub201-pAAV/Ad plasmid cotransfection system was developed to eliminate homologous recombination which leads to generation of the wild-type (wt) adeno-associated virus type 2 (AAV) during recombinant vector production. The extent of contamination with wt AAV has been documented to range between 0.01 and 10%. However, the precise mechanism of generation of the contaminating wt AAV remains unclear. To characterize the wt AAV genomes, recombinant viral stocks were used to infect human 293 cells in the presence of adenovirus. Southern blot analyses of viral replicative DNA intermedia

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Willaume, Simon, Emilie Rass, Paula Fontanilla-Ramirez, Angela Moussa, Paul Wanschoor, and Pascale Bertrand. "A Link between Replicative Stress, Lamin Proteins, and Inflammation." Genes 12, no. 4 (2021): 552. http://dx.doi.org/10.3390/genes12040552.

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Double-stranded breaks (DSB), the most toxic DNA lesions, are either a consequence of cellular metabolism, programmed as in during V(D)J recombination, or induced by anti-tumoral therapies or accidental genotoxic exposure. One origin of DSB sources is replicative stress, a major source of genome instability, especially when the integrity of the replication forks is not properly guaranteed. To complete stalled replication, restarting the fork requires complex molecular mechanisms, such as protection, remodeling, and processing. Recently, a link has been made between DNA damage accumulation and

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Gaurivaud, Patrice, Leonardo C. A. Souza, Andrea C. D. Virgílio, Anelise G. Mariano, Renê R. Palma, and Patrícia B. Monteiro. "Gene Disruption by Homologous Recombination in the Xylella fastidiosa Citrus Variegated Chlorosis Strain." Applied and Environmental Microbiology 68, no. 9 (2002): 4658–65. http://dx.doi.org/10.1128/aem.68.9.4658-4665.2002.

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ABSTRACT Mutagenesis by homologous recombination was evaluated in Xylella fastidiosa by using the bga gene, coding for β-galactosidase, as a model. Integration of replicative plasmids by homologous recombination between the cloned truncated copy of bga and the endogenous gene was produced by one or two crossover events leading to β-galactosidase mutants. A promoterless chloramphenicol acetyltransferase gene was used to monitor the expression of the target gene and to select a cvaB mutant.

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Slade, Dea. "Maneuvers on PCNA Rings during DNA Replication and Repair." Genes 9, no. 8 (2018): 416. http://dx.doi.org/10.3390/genes9080416.

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DNA replication and repair are essential cellular processes that ensure genome duplication and safeguard the genome from deleterious mutations. Both processes utilize an abundance of enzymatic functions that need to be tightly regulated to ensure dynamic exchange of DNA replication and repair factors. Proliferating cell nuclear antigen (PCNA) is the major coordinator of faithful and processive replication and DNA repair at replication forks. Post-translational modifications of PCNA, ubiquitination and acetylation in particular, regulate the dynamics of PCNA-protein interactions. Proliferating

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Lankenau, Susanne, Thorsten Barnickel, Joachim Marhold, Frank Lyko, Bernard M. Mechler, and Dirk-Henner Lankenau. "Knockout Targeting of the Drosophila Nap1 Gene and Examination of DNA Repair Tracts in the Recombination Products." Genetics 163, no. 2 (2003): 611–23. http://dx.doi.org/10.1093/genetics/163.2.611.

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Abstract We used ends-in gene targeting to generate knockout mutations of the nucleosome assembly protein 1 (Nap1) gene in Drosophila melanogaster. Three independent targeted null-knockout mutations were produced. No wild-type NAP1 protein could be detected in protein extracts. Homozygous Nap1KO knockout flies were either embryonic lethal or poorly viable adult escapers. Three additional targeted recombination products were viable. To gain insight into the underlying molecular processes we examined conversion tracts in the recombination products. In nearly all cases the I-SceI endonuclease sit

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Yip, Mitchell, Jing Chen, Yan Zhi, et al. "Querying Recombination Junctions of Replication-Competent Adeno-Associated Viruses in Gene Therapy Vector Preparations with Single Molecule, Real-Time Sequencing." Viruses 15, no. 6 (2023): 1228. http://dx.doi.org/10.3390/v15061228.

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Clinical-grade preparations of adeno-associated virus (AAV) vectors used for gene therapy typically undergo a series of diagnostics to determine titer, purity, homogeneity, and the presence of DNA contaminants. One type of contaminant that remains poorly investigated is replication-competent (rc)AAVs. rcAAVs form through recombination of DNA originating from production materials, yielding intact, replicative, and potentially infectious virus-like virions. They can be detected through the serial passaging of lysates from cells transduced by AAV vectors in the presence of wildtype adenovirus. Ce

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Cleaver, James E. "Mechanisms by which Human Cells Bypass Damaged Bases during DNA Replication after Ultraviolet Irradiation." Scientific World JOURNAL 2 (2002): 1296–305. http://dx.doi.org/10.1100/tsw.2002.348.

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The replication of damaged DNA involves cascading mechanisms of increasing complexity but decreasing accuracy. The most accurate mechanism uses low-fidelity DNA polymerases, Pol H and Pol I, which have active sites sufficiently large to accommodate a pyrimidine dimer. Replicative bypass of DNA damage by these polymerases produces an accurately replicated, newly synthesized strand. Pol H negative cells (XP-V cell lines) either adopt a proposed secondary bypass mechanism or a recombinational mode. The mechanism of the secondary bypass is unclear, but a number of experiments suggests roles for ex

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Tomso, Daniel J., and Kenneth N. Kreuzer. "Double-Strand Break Repair in Tandem Repeats During Bacteriophage T4 Infection." Genetics 155, no. 4 (2000): 1493–504. http://dx.doi.org/10.1093/genetics/155.4.1493.

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Abstract Recombinational repair of double-strand breaks in tandemly repeated sequences often results in the loss of one or more copies of the repeat. The single-strand annealing (SSA) model for repair has been proposed to account for this nonconservative recombination. In this study we present a plasmid-based physical assay that measures SSA during bacteriophage T4 infection and apply this assay to the genetic analysis of break repair. SSA occurs readily in broken plasmid DNA and is independent of the strand exchange protein UvsX and its accessory factor UvsY. We use the unique features of T4

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Kain, Alice Mac, Marie-Line Joffret, Francis Delpeyroux, Marco Vignuzzi, and Maël Bessaud. "A cold case: non-replicative recombination in positive-strand RNA viruses." Virologie 25, no. 4 (2021): 62–73. http://dx.doi.org/10.1684/vir.2021.0914.

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Kain, Alice Mac, Marie-Line Joffret, Francis Delpeyroux, Marco Vignuzzi, and Maël Bessaud. "A cold case: non-replicative recombination in positive-strand RNA viruses." Virologie 25, no. 4 (2021): 224–35. http://dx.doi.org/10.1684/vir.2021.0912.

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Hagelstrom, R. T., K. B. Blagoev, L. J. Niedernhofer, E. H. Goodwin, and S. M. Bailey. "Hyper telomere recombination accelerates replicative senescence and may promote premature aging." Proceedings of the National Academy of Sciences 107, no. 36 (2010): 15768–73. http://dx.doi.org/10.1073/pnas.1006338107.

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Pal, Sangita, Spike D. Postnikoff, Myrriah Chavez, and Jessica K. Tyler. "Impaired cohesion and homologous recombination during replicative aging in budding yeast." Science Advances 4, no. 2 (2018): eaaq0236. http://dx.doi.org/10.1126/sciadv.aaq0236.

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Duret, Sybille, Aurélie André, and Joël Renaudin. "Specific gene targeting in Spiroplasma citri: improved vectors and production of unmarked mutations using site-specific recombination." Microbiology 151, no. 8 (2005): 2793–803. http://dx.doi.org/10.1099/mic.0.28123-0.

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In Spiroplasma citri, where homologous recombination is inefficient, specific gene targeting could only be achieved by using replicative, oriC plasmids. To improve the probability of selecting rare recombination events without fastidious, extensive passaging of the transformants, a new targeting vector was constructed, which was used to inactivate the crr gene encoding the IIA component of the glucose phosphotransferase system (PTS) permease. Selection of recombinants was based on a two-step strategy using two distinct selection markers, one of which could only be expressed once recombination

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Smolikov, Sarit, and Anat Krauskopf. "The Rap1p-Telomere Complex Does Not Determine the Replicative Capacity of Telomerase-Deficient Yeast." Molecular and Cellular Biology 23, no. 23 (2003): 8729–39. http://dx.doi.org/10.1128/mcb.23.23.8729-8739.2003.

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ABSTRACT Telomeres are nucleoprotein structures that cap the ends of chromosomes and thereby protect their stability and integrity. In the presence of telomerase, the enzyme that synthesizes telomeric repeats, telomere length is controlled primarily by Rap1p, the budding yeast telomeric DNA binding protein which, through its C-terminal domain, nucleates a protein complex that limits telomere lengthening. In the absence of telomerase, telomeres shorten with every cell division, and eventually, cells enter replicative senescence. We have set out to identify the telomeric property that determines

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Zheng, Dao-Qiong, and Thomas Petes. "Genome Instability Induced by Low Levels of Replicative DNA Polymerases in Yeast." Genes 9, no. 11 (2018): 539. http://dx.doi.org/10.3390/genes9110539.

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Most cells of solid tumors have very high levels of genome instability of several different types, including deletions, duplications, translocations, and aneuploidy. Much of this instability appears induced by DNA replication stress. As a model for understanding this type of instability, we have examined genome instability in yeast strains that have low levels of two of the replicative DNA polymerases: DNA polymerase α and DNA polymerase δ (Polα and Polδ). We show that low levels of either of these DNA polymerases results in greatly elevated levels of mitotic recombination, chromosome rearrang

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Singh, Mayank, Clayton R. Hunt, Raj K. Pandita, et al. "Lamin A/C Depletion Enhances DNA Damage-Induced Stalled Replication Fork Arrest." Molecular and Cellular Biology 33, no. 6 (2013): 1210–22. http://dx.doi.org/10.1128/mcb.01676-12.

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The humanLMNAgene encodes the essential nuclear envelope proteins lamin A and C (lamin A/C). Mutations inLMNAresult in altered nuclear morphology, but how this impacts the mechanisms that maintain genomic stability is unclear. Here, we report that lamin A/C-deficient cells have a normal response to ionizing radiation but are sensitive to agents that cause interstrand cross-links (ICLs) or replication stress. In response to treatment with ICL agents (cisplatin, camptothecin, and mitomycin), lamin A/C-deficient cells displayed normal γ-H2AX focus formation but a higher frequency of cells with de

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Gibson, Ryan T., and Elliot J. Androphy. "The SMC5/6 Complex Represses the Replicative Program of High-Risk Human Papillomavirus Type 31." Pathogens 9, no. 10 (2020): 786. http://dx.doi.org/10.3390/pathogens9100786.

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The multi-subunit structural maintenance of chromosomes (SMC) 5/6 complex includes SMC6 and non-SMC element (NSE)3. SMC5/6 is essential for homologous recombination DNA repair and functions as an antiviral factor during hepatitis B (HBV) and herpes simplex-1 (HSV-1) viral infections. Intriguingly, SMC5/6 has been found to associate with high-risk human papillomavirus (HPV) E2 regulatory proteins, but the functions of this interaction and its role during HPV infection remain unclear. Here, we further characterize SMC5/6 interactions with HPV-31 E2 and its role in the HPV life cycle. Co-immunopr

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Clatterbuck Soper, Sarah F., and Paul S. Meltzer. "ATRX/DAXX: Guarding the Genome against the Hazards of ALT." Genes 14, no. 4 (2023): 790. http://dx.doi.org/10.3390/genes14040790.

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Proliferating cells must enact a telomere maintenance mechanism to ensure genomic stability. In a subset of tumors, telomeres are maintained not by telomerase, but through a homologous recombination-based mechanism termed Alternative Lengthening of Telomeres or ALT. The ALT process is linked to mutations in the ATRX/DAXX/H3.3 histone chaperone complex. This complex is responsible for depositing non-replicative histone variant H3.3 at pericentric and telomeric heterochromatin but has also been found to have roles in ameliorating replication in repeat sequences and in promoting DNA repair. In th

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Royle, Nicola J., Aarón Méndez-Bermúdez, Athanasia Gravani, et al. "The role of recombination in telomere length maintenance." Biochemical Society Transactions 37, no. 3 (2009): 589–95. http://dx.doi.org/10.1042/bst0370589.

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Human telomeres shorten during each cell division, predominantly because of incomplete DNA replication. This eventually results in short uncapped telomeres that elicit a DNA-damage response, leading to cellular senescence. However, evasion of senescence results in continued cell division and telomere erosion ultimately results in genome instability. In the long term, this genome instability is not sustainable, and cancer cells activate a TMM (telomere maintenance mechanism), either expression of telomerase or activation of the ALT (alternative lengthening of telomeres) pathway. Activation of t

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Brouillette, S., and P. Chartrand. "Intermolecular recombination assay for mammalian cells that produces recombinants carrying both homologous and nonhomologous junctions." Molecular and Cellular Biology 7, no. 6 (1987): 2248–55. http://dx.doi.org/10.1128/mcb.7.6.2248-2255.1987.

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We present an intermolecular recombination assay for mammalian cells that does not involve the reconstitution of a selectable marker. It is based on the generation of a shuttle vector by recombination between a bacterial and a mammalian vector. The recombinants can thus be amplified in mammalian cells, isolated by plasmid rescue in an Escherichia coli RecA- host, and identified by in situ hybridization, by using mammalian vector sequences as probes. Since both parental molecules can share defined lengths of homology, this assay permits a direct comparison between homologous and nonhomologous i

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Brouillette, S., and P. Chartrand. "Intermolecular recombination assay for mammalian cells that produces recombinants carrying both homologous and nonhomologous junctions." Molecular and Cellular Biology 7, no. 6 (1987): 2248–55. http://dx.doi.org/10.1128/mcb.7.6.2248.

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We present an intermolecular recombination assay for mammalian cells that does not involve the reconstitution of a selectable marker. It is based on the generation of a shuttle vector by recombination between a bacterial and a mammalian vector. The recombinants can thus be amplified in mammalian cells, isolated by plasmid rescue in an Escherichia coli RecA- host, and identified by in situ hybridization, by using mammalian vector sequences as probes. Since both parental molecules can share defined lengths of homology, this assay permits a direct comparison between homologous and nonhomologous i

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Zhao, Jiangning, Srikanth Talluri, Subodh Kumar, et al. "RAD51 Is Required for the Occupancy of Replication Licensing Factors on the Myeloma Genome." Blood 142, Supplement 1 (2023): 6587. http://dx.doi.org/10.1182/blood-2023-189307.

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Genomic instability and extended replicative potential arise early during oncogenic transformation and contribute to the development and progression of cancer. Although chromosomal instability and replication are distinct pathways, they share certain proteins and activities. DNA replication starts by sequential loading of replication licensing factors at replication origins. We have observed that RAD51 - a keystone protein in stabilizing the genome through homologous recombination (HR) and a dependency in multiple myeloma (MM) - interacts with the MCM complex. In fact, RAD51 knockdown inhibits

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Hagemann, A. T., and N. L. Craig. "Tn7 transposition creates a hotspot for homologous recombination at the transposon donor site." Genetics 133, no. 1 (1993): 9–16. http://dx.doi.org/10.1093/genetics/133.1.9.

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Abstract Homologous recombination at the bacterial transposon Tn7 donor site is stimulated 10-fold when Tn7 is activated to transpose at high frequency in RecD- Escherichia coli, where recombination is focused near the ends of double-chain breaks. This is observed as an increase in recombination between two lacZ heteroalleles when one copy of lacZ carries within it a Tn7 that is transposing at high frequency. This stimulation of recombination is dependent upon the presence of homology with the donor site, is independent of SOS induction, and is not due to a global stimulation of recombination.

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Spinnato, Maria Concetta, Alessandra Lo Sciuto, Jessica Mercolino, et al. "Effect of a Defective Clamp Loader Complex of DNA Polymerase III on Growth and SOS Response in Pseudomonas aeruginosa." Microorganisms 10, no. 2 (2022): 423. http://dx.doi.org/10.3390/microorganisms10020423.

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DNA polymerase III (Pol III) is the replicative enzyme in bacteria. It consists of three subcomplexes, the catalytic core, the β clamp, and the clamp loader. While this complex has been thoroughly characterized in the model organism Escherichia coli, much less is known about its functioning and/or its specific properties in other bacteria. Biochemical studies highlighted specific features in the clamp loader subunit ψ of Pseudomonas aeruginosa as compared to its E. coli counterpart, and transposon mutagenesis projects identified the ψ-encoding gene holD among the strictly essential core genes

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