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Journal articles on the topic 'Suppressed recombination'

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Published: 10 December 2022
Last updated: 28 January 2023

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1

Schild, D. "Suppression of a new allele of the yeast RAD52 gene by overexpression of RAD51, mutations in srs2 and ccr4, or mating-type heterozygosity." Genetics 140, no. 1 (May 1, 1995): 115–27. http://dx.doi.org/10.1093/genetics/140.1.115.

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Abstract The RAD52 gene of Saccharomyces cerevisiae is involved both in the recombinational repair of DNA damage and in mitotic and meiotic recombination. A new allele of rad52 has been isolated that has unusual properties. Unlike other alleles of rad52, this allele (rad52-20) is partially suppressed by an srs2 deletion; srs2 mutations normally act to suppress only rad6 and rad18 mutations. In addition, although haploid rad52-20 strains are very X-ray sensitive, diploids homozygous for this allele are only slightly X-ray sensitive and undergo normal meiosis and meiotic recombination. Because rad52-20 diploids homozygous for mating type are very X-ray sensitive, mating-type heterozygosity is acting to suppress rad52-20. Mating-type heterozygosity suppresses this allele even in haploids, because sir mutations, which result in expression of the normally silent mating-type cassettes, were identified among the extragenic revertants of rad52-20. A new allele of srs2 and alleles of the transcriptional regulatory genes ccr4 and caf1 were among the other extragenic revertants of rad52-20. Because other researchers have shown that the RAD51 and RAD52 proteins interact, RAD51 on a high copy number plasmid was tested and found to suppress the rad52-20 allele, but RAD54, 55 and 57 did not suppress. The RAD51 plasmid did not suppress rad52-1. The rad52-20 allele may encode a protein that has low affinity binding to the RAD51 protein. To test whether the selected revertants suppressed rad52-20 by elevating the expression of RAD51, an integrated RAD51-lacZ fusion was genetically crossed into each revertant. Because none of the revertants increased the level of RAD51-lacZ, the revertants must exert their effect by one or more mechanisms that are not mediated by RAD51.
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2

Milne, G. T., T. Ho, and D. T. Weaver. "Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51." Genetics 139, no. 3 (March 1, 1995): 1189–99. http://dx.doi.org/10.1093/genetics/139.3.1189.

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Abstract RAD52 function is required for virtually all DNA double-strand break repair and recombination events in Saccharomyces cerevisiae. To gain greater insight into the mechanism of RAD52-mediated repair, we screened for genes that suppress partially active alleles of RAD52 when mutant or overexpressed. Described here is the isolation of a phenotypic null allele of SRS2 that suppressed multiple alleles of RAD52 (rad52B, rad52D, rad52-1 and KlRAD52) and RAD51 (KlRAD51) but failed to suppress either a rad52 delta or a rad51 delta. These results indicate that SRS2 antagonizes RAD51 and RAD52 function in recombinational repair. The mechanism of suppression of RAD52 alleles by srs2 is distinct from that which has been previously described for RAD51 overexpression, as both conditions were shown to act additively with respect to the rad52B allele. Furthermore, overexpression of either RAD52 or RAD51 enhanced the recombination-dependent sensitivity of an srs2 delta RAD52 strain, suggesting that RAD52 and RAD51 positively influence recombinational repair mechanisms. Thus, RAD52-dependent recombinational repair is controlled both negatively and positively.
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3

Lewis, L. Kevin, G. Karthikeyan, James W. Westmoreland, and Michael A. Resnick. "Differential Suppression of DNA Repair Deficiencies of Yeast rad50, mre11 and xrs2 Mutants by EXO1 and TLC1 (the RNA Component of Telomerase)." Genetics 160, no. 1 (January 1, 2002): 49–62. http://dx.doi.org/10.1093/genetics/160.1.49.

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Abstract Rad50, Mre11, and Xrs2 form a nuclease complex that functions in both nonhomologous end-joining (NHEJ) and recombinational repair of DNA double-strand breaks (DSBs). A search for highly expressed cDNAs that suppress the DNA repair deficiency of rad50 mutants yielded multiple isolates of two genes: EXO1 and TLC1. Overexpression of EXO1 or TLC1 increased the resistance of rad50, mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase resistance in strains defective in recombination (rad51, rad52, rad54, rad59) or NHEJ only (yku70, sir4). Increased Exo1 or TLC1 RNA did not alter checkpoint responses or restore NHEJ proficiency, but DNA repair defects of yku70 and rad27 (fen) mutants were differentially suppressed by the two genes. Overexpression of Exo1, but not mutant proteins containing substitutions in the conserved nuclease domain, increased recombination and suppressed HO and EcoRI endonuclease-induced killing of rad50 strains. exo1 rad50 mutants lacking both nuclease activities exhibited a high proportion of enlarged, G2-arrested cells and displayed a synergistic decrease in DSB-induced plasmid:chromosome recombination. These results support a model in which the nuclease activity of the Rad50/Mre11/Xrs2 complex is required for recombinational repair, but not NHEJ. We suggest that the 5′–3′ exo activity of Exo1 is able to substitute for Rad50/Mre11/Xrs2 in rescission of specific classes of DSB end structures. Gene-specific suppression by TLC1, which encodes the RNA subunit of the yeast telomerase complex, demonstrates that components of telomerase can also impact on DSB repair pathways.
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4

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 (August 1, 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) suppress SV40-induced homologous recombination to the extent that they suppress DNA synthesis. Stable integration of plasmids encoding T antigen also augments homologous recombination, which is suppressed by aphidicolin. We infer that the mechanism by which T antigen stimulates homologous recombination in human fibroblasts involves DNA replicative synthesis.
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5

Nanbu, Tomoko, Katsunori Takahashi, Johanne M. Murray, Naoya Hirata, Shinobu Ukimori, Mai Kanke, Hisao Masukata, Masashi Yukawa, Eiko Tsuchiya, and Masaru Ueno. "Fission Yeast RecQ Helicase Rqh1 Is Required for the Maintenance of Circular Chromosomes." Molecular and Cellular Biology 33, no. 6 (January 7, 2013): 1175–87. http://dx.doi.org/10.1128/mcb.01713-12.

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Protection of telomeres protein 1 (Pot1) binds to single-stranded telomere overhangs and protects chromosome ends. RecQ helicases regulate homologous recombination at multiple stages, including resection, strand displacement, and resolution. Fission yeastpot1and RecQ helicaserqh1double mutants are synthetically lethal, but the mechanism is not fully understood. Here, we show that the synthetic lethality ofpot1Δrqh1Δ double mutants is due to inappropriate homologous recombination, as it is suppressed by the deletion ofrad51+. The expression of Rad51 in thepot1Δrqh1Δrad51Δ triple mutant, which has circular chromosomes, is lethal. Reduction of the expression of Rqh1 in apot1disruptant with circular chromosomes caused chromosome missegregation, and this defect was partially suppressed by the deletion ofrad51+. Taken together, our results suggest that Rqh1 is required for the maintenance of circular chromosomes when homologous recombination is active. Crossovers between circular monomeric chromosomes generate dimers that cannot segregate properly inEscherichia coli. We propose that Rqh1 inhibits crossovers between circular monomeric chromosomes to suppress the generation of circular dimers.
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6

Charlesworth, Deborah, Roberta Bergero, Chay Graham, Jim Gardner, and Karen Keegan. "How did the guppy Y chromosome evolve?" PLOS Genetics 17, no. 8 (August 9, 2021): e1009704. http://dx.doi.org/10.1371/journal.pgen.1009704.

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The sex chromosome pairs of many species do not undergo genetic recombination, unlike the autosomes. It has been proposed that the suppressed recombination results from natural selection favouring close linkage between sex-determining genes and mutations on this chromosome with advantages in one sex, but disadvantages in the other (these are called sexually antagonistic mutations). No example of such selection leading to suppressed recombination has been described, but populations of the guppy display sexually antagonistic mutations (affecting male coloration), and would be expected to evolve suppressed recombination. In extant close relatives of the guppy, the Y chromosomes have suppressed recombination, and have lost all the genes present on the X (this is called genetic degeneration). However, the guppy Y occasionally recombines with its X, despite carrying sexually antagonistic mutations. We describe evidence that a new Y evolved recently in the guppy, from an X chromosome like that in these relatives, replacing the old, degenerated Y, and explaining why the guppy pair still recombine. The male coloration factors probably arose after the new Y evolved, and have already evolved expression that is confined to males, a different way to avoid the conflict between the sexes.
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7

Poteete, Anthony R. "Modulation of DNA Repair and Recombination by the Bacteriophage λ Orf Function in Escherichia coli K-12." Journal of Bacteriology 186, no. 9 (May 1, 2004): 2699–707. http://dx.doi.org/10.1128/jb.186.9.2699-2707.2004.

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ABSTRACT The orf gene of bacteriophage λ, fused to a promoter, was placed in the galK locus of Escherichia coli K-12. Orf was found to suppress the recombination deficiency and sensitivity to UV radiation of mutants, in a Δ(recC ptr recB recD)::P tac gam bet exo pae cI ΔrecG background, lacking recF, recO, recR, ruvAB, and ruvC functions. It also suppressed defects of these mutants in establishing replication of a pSC101-related plasmid. Compared to orf, the recA803 allele had only small effects on recF, recO, and recR mutant phenotypes and no effect on a ruvAB mutant. In a fully wild-type background with respect to known recombination and repair functions, orf partially suppressed the UV sensitivity of ruvAB and ruvC mutants.
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8

Feng, Zichao, Ruina Ma, An Du, Yinan Zhang, Xue Zhao, Yongzhe Fan, and Xiaoming Cao. "Enhanced Performance of Near-Infrared-Absorption CdSeTe Quantum Dot-Sensitized Solar Cells Via Octa-Aminopropyl Polyhedral Oligomeric Silsesquioxane Modification." Nano 14, no. 07 (July 2019): 1950087. http://dx.doi.org/10.1142/s1793292019500875.

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The charge recombination caused by surface defects limits photovoltaic properties of quantum dot-sensitized solar cells (QDSSCs), which can be suppressed by modifying organic or inorganic molecules and atomic ligands. In this paper, octa-aminopropyl polyhedral oligomeric silsesquioxane (OA-POSS) connected and modified near-infrared absorption CdSeTe quantum dots (QDs) through coupling agent (1-ethyl-3-3-dimethylaminopropyl carbodiimide hydrochloride). The results suggest that OA-POSS reduces the surface defects of CdSeTe QDs and suppresses charge recombination. Therefore, the power conversion efficiency improves nearly 41%, which increases from 2.00% to 2.82%.
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9

Olson, M. V., A. Kas, K. Bubb, R. Qui, E. E. Smith, C. K. Raymond, and R. Kaul. "Hypervariability, suppressed recombination and the genetics of individuality." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (January 29, 2004): 129–40. http://dx.doi.org/10.1098/rstb.2003.1418.

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We define ‘genetic individuality’ as intraspecies variation that has substantial heritability and involves traits that are sufficiently common that they can be observed in any modest–sized sampling of individuals. We propose that genetic individuality is largely shaped by the combinatory shuffling of a modest number of genes, each of which exists as a family of functionally and structurally diverged alleles. Unequivocal examples of such allele families are found at the O–antigen–biosynthetic locus in Pseudomonas aeruginosa and the human leucocyte antigen locus in humans. We examine characteristic features of these allele families and explore the possibility that genetic loci with similar characteristics can be recognized in a whole–genome scan of human genetic variation.
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10

Shulman, M. J., C. Collins, A. Connor, L. R. Read, and M. D. Baker. "Interchromosomal recombination is suppressed in mammalian somatic cells." EMBO Journal 14, no. 16 (August 1995): 4102–7. http://dx.doi.org/10.1002/j.1460-2075.1995.tb00082.x.

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11

Stark, Jeremy M., and Maria Jasin. "Extensive Loss of Heterozygosity Is Suppressed during Homologous Repair of Chromosomal Breaks." Molecular and Cellular Biology 23, no. 2 (January 15, 2003): 733–43. http://dx.doi.org/10.1128/mcb.23.2.733-743.2003.

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ABSTRACT Loss of heterozygosity (LOH) is a common genetic alteration in tumors and often extends several megabases to encompass multiple genetic loci or even whole chromosome arms. Based on marker and karyotype analysis of tumor samples, a significant fraction of LOH events appears to arise from mitotic recombination between homologous chromosomes, reminiscent of recombination during meiosis. As DNA double-strand breaks (DSBs) initiate meiotic recombination, a potential mechanism leading to LOH in mitotically dividing cells is DSB repair involving homologous chromosomes. We therefore sought to characterize the extent of LOH arising from DSB-induced recombination between homologous chromosomes in mammalian cells. To this end, a recombination reporter was introduced into a mouse embryonic stem cell line that has nonisogenic maternal and paternal chromosomes, as is the case in human populations, and then a DSB was introduced into one of the chromosomes. Recombinants involving alleles on homologous chromosomes were readily obtained at a frequency of 4.6 × 10−5; however, this frequency was substantially lower than that of DSB repair by nonhomologous end joining or the inferred frequency of homologous repair involving sister chromatids. Strikingly, the majority of recombinants had LOH restricted to the site of the DSB, with a minor class of recombinants having LOH that extended to markers 6 kb from the DSB. Furthermore, we found no evidence of LOH extending to markers 1 centimorgan or more from the DSB. In addition, crossing over, which can lead to LOH of a whole chromosome arm, was not observed, implying that there are key differences between mitotic and meiotic recombination mechanisms. These results indicate that extensive LOH is normally suppressed during DSB-induced allelic recombination in dividing mammalian cells.
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12

Lovett, Susan T., and Robert K. Mortimer. "Characterization of Null Mutants of the RAD55 Gene of Saccharomyces cerevisiae: Effects of Temperature, Osmotic Strength and Mating Type." Genetics 116, no. 4 (August 1, 1987): 547–53. http://dx.doi.org/10.1093/genetics/116.4.547.

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ABSTRACT RAD55 belongs to a group of genes required for resistance to ionizing radiation, RAD50-RAD57, which are thought to define a pathway of recombinational repair. Since all four alleles of RAD55 are temperature conditional (cold sensitive) for their radiation phenotype, we investigated the phenotype produced by null mutations in the RAD55 gene, constructed in vitro and transplaced to the yeast chromosome. The X-ray sensitivity of these null mutant strains was surprisingly suppressed by increased temperature, osmotic strength of the growth medium and heterozygosity at the mating-type locus. These first two properties, temperature conditionality and osmotic remediability, are commonly associated with missense mutations; these rad55 null mutants are unique in that they exhibit these properties although the mutant gene cannot be expressed. X-ray-induced mitotic recombination was also cold sensitive in rad55 mutant diploids. Although mitotic growth was unaffected in these strains, meiosis was a lethal event at both high and low temperatures. Whereas the phenotype of rad55 null mutants is consistent with a role of RAD55 in recombination and recombinational repair, there is evidence for considerable RAD55-independent recombination, at least in mitotic cells, which is influenced by temperature and MAT. We discuss models for the role of RAD55 in recombination to explain the unusual properties of rad55 mutants.
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13

Mendonca, V. M., and S. W. Matson. "Genetic analysis of delta helD and delta uvrD mutations in combination with other genes in the RecF recombination pathway in Escherichia coli: suppression of a ruvB mutation by a uvrD deletion." Genetics 141, no. 2 (October 1, 1995): 443–52. http://dx.doi.org/10.1093/genetics/141.2.443.

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Abstract Helicase II (uvrD gene product) and helicase IV (helD gene product) have been shown previously to be involved in the RecF pathway of recombination. To better understand the role of these two proteins in homologous recombination in the RecF pathway [recBCsbcB(C) background, we investigated the interactions between helD, uvrD and the following RecF pathway genes: recF, recO, recN and ruvAB. We observed synergistic interactions between uvrD ant the recF, recN, recO and recG genes in both conjugational recombination and the repair of methylmethane sulfonate (MMS)-induced DNA damage. No synergistic interactions were detected between helD and the recF, recO and regN genes when conjugational recombination was analyzed. We did, however, detect synergistic interactions between helD and recF/recO in recombinational repair. Surprisingly, the uvrD deletion completely suppressed the phenotype of a ruvB mutation in a recBCsbcB(C) background. Both conjugational recombination efficiency and MMS-damaged DNA repair proficiency returned to wild-type levels in the deltauvrDruvB9 double mutant. Suppression of the effects of the ruvB mutation by a uvrD deletion was dependent on the recG and recN genes and not dependent on the recF/O/R genes. These data are discussed in the context of two "RecF" homologous recombination pathways operating in a recBCsbcB(C) strain background.
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14

Nadeau, Joseph H. "Length of the chromosomal segment marked by galactose-1-phosphate uridyl transferase and soluble aconitase and conserved since divergence of lineages leading to mouse and man." Genetical Research 52, no. 2 (October 1988): 141–44. http://dx.doi.org/10.1017/s0016672300027518.

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SummaryStandard linkage testing crosses and ovarian teratoma mapping were used to estimate the length of the chromosomal segment that is marked by galactose-1-phosphate uridyl transferase and soluble aconitase and that has been conserved since divergence of lineages leading to mouse and man. These experiments were also used to determine whether the Rb(4·6)2Bnr Robertsonian translocation suppresses recombination on the proximal portion of mouse Chromosome 4. The estimated length of the conserved segment marked by galactose-1-phosphate uridyl transferase and soluble aconitase in mouse and man was estimated to be 24 cM. It was also shown that Rb(4·6)2Bnr strongly suppressed recombination on the centromeric portion of mouse Chromosome 4.
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15

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

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Abstract Mutations of Escherichia coli K-12 were isolated that increase the frequency of deletion formation. Three of these mutations map to the gene sbcB at 43.5 min on the E. coli chromosome. Two types of mutations at sbcB have been previously defined: sbcB-type that suppress both the UV sensitivity and recombination deficiency of recBC mutants, and xonA-type that suppress only the UV sensitivity. Both types are defective for production of exonuclease I activity. The mutations isolated here were similar to xonA alleles of sbcB because they suppressed the UV sensitivity of recBC mutants but did not restore recombination proficiency. Indeed, two previously characterized xonA alleles were shown to increase the frequency of deletion formation, although an sbcB allele did not. This result demonstrates that loss of exonuclease I activity is not sufficient to confer a high deletion phenotype, rather, the product of the sbcB gene possesses some other function that is important for deletion formation. Because deletion formation in this system is recA independent and does not require extensive DNA homology, these mutations affect a pathway of illegitimate recombination.
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16

Neu, Christina, Nils Stein, and Beat Keller. "Genetic mapping of the Lr20–Pm1 resistance locus reveals suppressed recombination on chromosome arm 7AL in hexaploid wheat." Genome 45, no. 4 (August 1, 2002): 737–44. http://dx.doi.org/10.1139/g02-040.

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The Lr20–Sr15–Pm1 resistance locus in hexaploid wheat confers resistance to three different fungal wheat pathogens (leaf rust, stem rust, and powdery mildew). It was previously localized in the distal region of chromosome arm 7AL. As a first step towards the isolation of this complex locus, we performed molecular mapping of the Lr20 and Pm1 genes in three F2 populations. In two populations, a cluster of 8 and 12 markers, respectively, cosegregated with the resistance genes. In a third population based on a cross between a susceptible lr20 mutant and a resistant cultivar, all clustered markers were monomorphic. However, in this population the recombination frequency proximal to the Lr20 gene was up to 60 times higher, indicating that the complete genetic linkage of the clustered markers is not due to a close physical linkage of the probes but is caused by suppressed recombination. This was supported by the analysis of Triticum monococcum BAC clones where no physical linkage between cosegregating probes was observed. Suppressed recombination at the Lr20–Pm1 locus is likely the result of an alien introgression of chromatin from an unidentified wild relative species or is due to chromosomal rearrangements.Key words: wheat, leaf rust, powdery mildew, resistance, suppressed recombination.
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17

Kawamata, Toyotaka, Jun Lu, Tadayuki Sato, Masafumi Tanaka, Hitoshi Nagaoka, Yasutoshi Agata, Takae Toyoshima, et al. "Imatinib mesylate directly impairs class switch recombination through down-regulation of AID: its potential efficacy as an AID suppressor." Blood 119, no. 13 (March 29, 2012): 3123–27. http://dx.doi.org/10.1182/blood-2011-01-327932.

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Abstract Activation-induced cytidine deaminase (AID) is essential for class switch recombination and somatic hypermutation. Its deregulated expression acts as a genomic mutator that can contribute to the development of various malignancies. During treatment with imatinib mesylate (IM), patients with chronic myeloid leukemia often develop hypogammaglobulinemia, the mechanism of which has not yet been clarified. Here, we provide evidence that class switch recombination on B-cell activation is apparently inhibited by IM through down-regulation of AID. Furthermore, expression of E2A, a key transcription factor for AID induction, was markedly suppressed by IM. These results elucidate not only the underlying mechanism of IM-induced hypogammaglobulinemia but also its potential efficacy as an AID suppressor.
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18

Villoutreix, Romain, Clarissa F. de Carvalho, Víctor Soria-Carrasco, Dorothea Lindtke, Marisol De-la-Mora, Moritz Muschick, Jeffrey L. Feder, Thomas L. Parchman, Zach Gompert, and Patrik Nosil. "Large-scale mutation in the evolution of a gene complex for cryptic coloration." Science 369, no. 6502 (July 23, 2020): 460–66. http://dx.doi.org/10.1126/science.aaz4351.

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The types of mutations affecting adaptation in the wild are only beginning to be understood. In particular, whether structural changes shape adaptation by suppressing recombination or by creating new mutations is unresolved. Here, we show that multiple linked but recombining loci underlie cryptic color morphs of Timema chumash stick insects. In a related species, these loci are found in a region of suppressed recombination, forming a supergene. However, in seven species of Timema, we found that a megabase-size “supermutation” has deleted color loci in green morphs. Moreover, we found that balancing selection likely contributes more to maintaining this mutation than does introgression. Our results show how suppressed recombination and large-scale mutation can help to package gene complexes into discrete units of diversity such as morphs, ecotypes, or species.
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19

Beam, Cynthia E., Catherine J. Saveson, and Susan T. Lovett. "Role for radA/sms in Recombination Intermediate Processing in Escherichia coli." Journal of Bacteriology 184, no. 24 (December 15, 2002): 6836–44. http://dx.doi.org/10.1128/jb.184.24.6836-6844.2002.

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ABSTRACT RadA/Sms is a highly conserved eubacterial protein that shares sequence similarity with both RecA strand transferase and Lon protease. We examined mutations in the radA/sms gene of Escherichia coli for effects on conjugational recombination and sensitivity to DNA-damaging agents, including UV irradiation, methyl methanesulfonate (MMS), mitomycin C, phleomycin, hydrogen peroxide, and hydroxyurea (HU). Null mutants of radA were modestly sensitive to the DNA-methylating agent MMS and to the DNA strand breakage agent phleomycin, with conjugational recombination decreased two- to threefold. We combined a radA mutation with other mutations in recombination genes, including recA, recB, recG, recJ, recQ, ruvA, and ruvC. A radA mutation was strongly synergistic with the recG Holliday junction helicase mutation, producing profound sensitivity to all DNA-damaging agents tested. Lesser synergy was noted between a mutation in radA and recJ, recQ, ruvA, ruvC, and recA for sensitivity to various genotoxins. For survival after peroxide and HU exposure, a radA mutation surprisingly suppressed the sensitivity of recA and recB mutants, suggesting that RadA may convert some forms of damage into lethal intermediates in the absence of these functions. Loss of radA enhanced the conjugational recombination deficiency conferred by mutations in Holliday junction-processing function genes, recG, ruvA, and ruvC. A radA recG ruv triple mutant had severe recombinational defects, to the low level exhibited by recA mutants. These results establish a role for RadA/Sms in recombination and recombinational repair, most likely involving the stabilization or processing of branched DNA molecules or blocked replication forks because of its genetic redundancy with RecG and RuvABC.
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20

García-Santamaría, Florencio, Yongfen Chen, Javier Vela, Richard D. Schaller, Jennifer A. Hollingsworth, and Victor I. Klimov. "Suppressed Auger Recombination in “Giant” Nanocrystals Boosts Optical Gain Performance." Nano Letters 9, no. 10 (October 14, 2009): 3482–88. http://dx.doi.org/10.1021/nl901681d.

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21

Tempelaar, Roel, L. Jan Anton Koster, Remco W. A. Havenith, Jasper Knoester, and Thomas L. C. Jansen. "Charge Recombination Suppressed by Destructive Quantum Interference in Heterojunction Materials." Journal of Physical Chemistry Letters 7, no. 1 (December 30, 2015): 198–203. http://dx.doi.org/10.1021/acs.jpclett.5b02580.

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22

Si, Wenping, Fatima Haydous, Ugljesa Babic, Daniele Pergolesi, and Thomas Lippert. "Suppressed Charge Recombination in Hematite Photoanode via Protonation and Annealing." ACS Applied Energy Materials 2, no. 8 (June 13, 2019): 5438–45. http://dx.doi.org/10.1021/acsaem.9b00420.

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23

Lenz, O., U. Teichmann, A. Langers, L. J. Striker, and G. E. Striker *, ‡ , W.J. Pavan. "Linkage disequilibrium mapping reveals suppressed recombination at the Os locus." Mammalian Genome 9, no. 8 (August 1, 1998): 681–82. http://dx.doi.org/10.1007/s003359900847.

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24

Trickey, Michelle, Margaret Grimaldi, and Hiroyuki Yamano. "The Anaphase-Promoting Complex/Cyclosome Controls Repair and Recombination by Ubiquitylating Rhp54 in Fission Yeast." Molecular and Cellular Biology 28, no. 12 (April 21, 2008): 3905–16. http://dx.doi.org/10.1128/mcb.02116-07.

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ABSTRACT Homologous recombination (HR) is important for maintaining genome integrity and for the process of meiotic chromosome segregation and the generation of variation. HR is regulated throughout the cell cycle, being prevalent in the S and G2 phases and suppressed in the G1 phase. Here we show that the anaphase-promoting complex/cyclosome (APC/C) regulates homologous recombination in the fission yeast Schizosaccharomyces pombe by ubiquitylating Rhp54 (an ortholog of Rad54). We show that Rhp54 is a novel APC/C substrate that is destroyed in G1 phase in a KEN-box- and Ste9/Fizzy-related manner. The biological consequences of failing to temporally regulate HR via Rhp54 degradation are seen in haploid cells only in the absence of antirecombinase Srs2 function and are more extensive in diploid cells, which become sensitive to a range of DNA-damaging agents, including hydroxyurea, methyl methanesulfonate, bleomycin, and UV. During meiosis, expression of nondegradable Rhp54 inhibits interhomolog recombination and stimulates sister chromatid recombination. We thus propose that it is critical to control levels of Rhp54 in G1 to suppress HR repair of double-strand breaks and during meiosis to coordinate interhomolog recombination.
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Shinohara, Miki, Kazuko Sakai, Akira Shinohara, and Douglas K. Bishop. "Crossover Interference in Saccharomyces cerevisiae Requires a TID1/RDH54- and DMC1-Dependent Pathway." Genetics 163, no. 4 (April 1, 2003): 1273–86. http://dx.doi.org/10.1093/genetics/163.4.1273.

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Abstract Two RecA-like recombinases, Rad51 and Dmc1, function together during double-strand break (DSB)-mediated meiotic recombination to promote homologous strand invasion in the budding yeast Saccharomyces cerevisiae. Two partially redundant proteins, Rad54 and Tid1/Rdh54, act as recombinase accessory factors. Here, tetrad analysis shows that mutants lacking Tid1 form four-viable-spore tetrads with levels of interhomolog crossover (CO) and noncrossover recombination similar to, or slightly greater than, those in wild type. Importantly, tid1 mutants show a marked defect in crossover interference, a mechanism that distributes crossover events nonrandomly along chromosomes during meiosis. Previous work showed that dmc1Δ mutants are strongly defective in strand invasion and meiotic progression and that these defects can be partially suppressed by increasing the copy number of RAD54. Tetrad analysis is used to show that meiotic recombination in RAD54-suppressed dmc1Δ cells is similar to that in tid1; the frequency of COs and gene conversions is near normal, but crossover interference is defective. These results support the proposal that crossover interference acts at the strand invasion stage of recombination.
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26

Maeda, T., H. Sugiyama, Y. Tani, and S. Kishimoto. "The DJH complex remains active in recombination to VH segments after the loss of mu-chain expression in mu-positive pre-B cells." Journal of Immunology 142, no. 10 (May 15, 1989): 3652–56. http://dx.doi.org/10.4049/jimmunol.142.10.3652.

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Abstract AT11-2 is an Abelson virus-transformed B precursor cell line which is capable of differentiating Ig- from mu+ cells via functional recombination of VH segments to preexisting DJH complexes. We describe here that after a mu+ subclone (VDJ+/DJ) generated from Ig- AT11-2 (DJ/DJ) cells by in vitro functional VH to DJH recombination subsequently lost mu-chain expression either by the recombination of a pseudo VH segment to the VHDJH+ allele or by the deletion of VHDJH+ allele, a novel productive joining of VH segments to the preexisting DJH complex occurred. These results indicated that VH to VHDJH rearrangement was not suppressed in mu-chain producing cells and that the DJH complexes still remained active in the recombination to VH segments after the loss of mu-chain expression. Our results may also suggest that VH to DJH rearrangement, but not VH to VHDJH rearrangement, is suppressed in mu-chain producing cells to maintain allelic exclusion. Our cell differentiation system should continue to be valuable for elucidating the mechanism of suppression and associated implications regarding allelic exclusion.
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27

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 (July 1, 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 (AlkA) DNA glycosylase. These results suggest that Ung and Fpg remove nontoxic NO.-induced base damage to create BER intermediates that are toxic if they are not processed by AP endonucleases. Our next goal was to learn how Ung and Fpg affect susceptibility to homologous recombination. The RecBCD complex is critical for repair of double-strand breaks via homologous recombination. When both Ung and Fpg were inactivated in recBCD cells, survival was significantly enhanced. We infer that both Ung and Fpg create substrates for recombinational repair, which is consistent with the observation that disrupting ung and fpg suppressed NO.-induced recombination. Taken together, a picture emerges in which the action of DNA glycosylases on NO.-induced base damage results in the accumulation of BER intermediates, which in turn can induce homologous recombination. These studies shed light on the underlying mechanism of NO.-induced homologous recombination.
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28

McKim, K. S., A. M. Howell, and A. M. Rose. "The effects of translocations on recombination frequency in Caenorhabditis elegans." Genetics 120, no. 4 (December 1, 1988): 987–1001. http://dx.doi.org/10.1093/genetics/120.4.987.

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Abstract In the nematode Caenorhabditis elegans, recombination suppression in translocation heterozygotes is severe and extensive. We have examined the meiotic properties of two translocations involving chromosome I, szT1(I;X) and hT1(I;V). No recombination was observed in either of these translocation heterozygotes along the left (let-362-unc-13) 17 map units of chromosome I. Using half-translocations as free duplications, we mapped the breakpoints of szT1 and hT1. The boundaries of crossover suppression coincided with the physical breakpoints. We propose that DNA sequences at the right end of chromosome I facilitate pairing and recombination. We use the data from translocations of other chromosomes to map the location of pairing sites on four other chromosomes. hT1 and szT1 differed markedly in their effect on recombination adjacent to the crossover suppressed region. hT1 had no effect on recombination in the adjacent interval. In contrast, the 0.8 map unit interval immediately adjacent to the szT1(I;X) breakpoint on chromosome I increased to 2.5 map units in translocation heterozygotes. This increase occurs in a chromosomal interval which can be expanded by treatment with radiation. These results are consistent with the suggestion that the szT1(I) breakpoint is in a region of DNA in which meiotic recombination is suppressed relative to the genomic average. We propose that DNA sequences disrupted by the szT1 translocation are responsible for determining the frequency of meiotic recombination in the vicinity of the breakpoint.
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29

Carey, Sarah B., Jerry Jenkins, John T. Lovell, Florian Maumus, Avinash Sreedasyam, Adam C. Payton, Shengqiang Shu, et al. "Gene-rich UV sex chromosomes harbor conserved regulators of sexual development." Science Advances 7, no. 27 (June 2021): eabh2488. http://dx.doi.org/10.1126/sciadv.abh2488.

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Nonrecombining sex chromosomes, like the mammalian Y, often lose genes and accumulate transposable elements, a process termed degeneration. The correlation between suppressed recombination and degeneration is clear in animal XY systems, but the absence of recombination is confounded with other asymmetries between the X and Y. In contrast, UV sex chromosomes, like those found in bryophytes, experience symmetrical population genetic conditions. Here, we generate nearly gapless female and male chromosome-scale reference genomes of the moss Ceratodon purpureus to test for degeneration in the bryophyte UV sex chromosomes. We show that the moss sex chromosomes evolved over 300 million years ago and expanded via two chromosomal fusions. Although the sex chromosomes exhibit weaker purifying selection than autosomes, we find that suppressed recombination alone is insufficient to drive degeneration. Instead, the U and V sex chromosomes harbor thousands of broadly expressed genes, including numerous key regulators of sexual development across land plants.
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30

Cano, David A., M. Graciela Pucciarelli, Francisco García-del Portillo, and Josep Casadesús. "Role of the RecBCD Recombination Pathway in Salmonella Virulence." Journal of Bacteriology 184, no. 2 (January 15, 2002): 592–95. http://dx.doi.org/10.1128/jb.184.2.592-595.2002.

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ABSTRACT Mutants of Salmonella enterica lacking the RecBC function are avirulent in mice and unable to grow inside macrophages (N. A. Buchmeier, C. J. Lipps, M. Y. H. So, and F. Heffron, Mol. Microbiol. 7:933–936, 1993). The virulence-related defects of RecBC− mutants are not suppressed by sbcB and sbcCD mutations, indicating that activation of the RecF recombination pathway cannot replace the virulence-related function(s) of RecBCD. Functions of the RecF pathway such as RecJ and RecF are not required for virulence. Since the RecBCD pathway, but not the RecF pathway, is known to participate in the repair of double-strand breaks produced during DNA replication, we propose that systemic infection by S. enterica may require RecBCD-mediated recombinational repair to prime DNA replication inside phagocytes. Mutants lacking both RecD and RecJ are also attenuated in mice and are unable to proliferate in macrophages, suggesting that exonucleases V and IX provide alternative functions for RecBCD-mediated recombinational repair during Salmonella infection.
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Huang, Jianting, Jinting Li, Linqi Zheng, Guohui Zhong, Yafeng Li, Junming Li, and Mingdeng Wei. "Defect passivation of a perovskite film by ZnIn2S4 nanosheets for efficient and stable perovskite solar cells." Chemical Communications 58, no. 5 (2022): 653–56. http://dx.doi.org/10.1039/d1cc06071f.

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32

Zeng, Kaiwen, Weiqiang Tang, Chengjie Li, Yingying Chen, Shuangliang Zhao, Qingyun Liu, and Yongshu Xie. "Systematic optimization of the substituents on the phenothiazine donor of doubly strapped porphyrin sensitizers: an efficiency over 11% unassisted by any cosensitizer or coadsorbent." Journal of Materials Chemistry A 7, no. 36 (2019): 20854–60. http://dx.doi.org/10.1039/c9ta06911a.

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Charge recombination was effectively suppressed by judicious optimization of the substituents of the phenothiazine donor, and the power conversion efficiency was successfully improved from 9.3% to 11.1%.
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33

Fuller, Zachary L., Spencer A. Koury, Christopher J. Leonard, Randee E. Young, Kobe Ikegami, Jonathan Westlake, Stephen Richards, Stephen W. Schaeffer, and Nitin Phadnis. "Extensive Recombination Suppression and Epistatic Selection Causes Chromosome-Wide Differentiation of a Selfish Sex Chromosome in Drosophila pseudoobscura." Genetics 216, no. 1 (July 30, 2020): 205–26. http://dx.doi.org/10.1534/genetics.120.303460.

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Sex-Ratio (SR) chromosomes are selfish X-chromosomes that distort Mendelian segregation and are commonly associated with inversions. These chromosomal rearrangements suppress recombination with Standard (ST) X-chromosomes and are hypothesized to maintain multiple alleles important for distortion in a single large haplotype. Here, we conduct a multifaceted study of the multiply inverted Drosophila pseudoobscura SR chromosome to understand the evolutionary history, genetic architecture, and present-day dynamics that shape this enigmatic selfish chromosome. The D. pseudoobscura SR chromosome has three nonoverlapping inversions of the right arm of the metacentric X-chromosome: basal, medial, and terminal. We find that 23 of 29 Mb of the D. pseudoobscuraX-chromosome right arm is highly differentiated between the Standard and SR arrangements, including a 6.6 Mb collinear region between the medial and terminal inversions. Although crossing-over is heavily suppressed on this chromosome arm, we discover it is not completely eliminated, with measured rates indicating recombination suppression alone cannot explain patterns of differentiation or the near-perfect association of the three SR chromosome inversions in nature. We then demonstrate the ancient basal and medial inversions of the SR chromosome contain genes sufficient to cause weak distortion. In contrast, the younger terminal inversion cannot distort by itself, but contains at least one modifier gene necessary for full manifestation of strong sex chromosome distortion. By parameterizing population genetic models for chromosome-wide linkage disequilibrium with our experimental results, we infer that strong selection acts to maintain the near-perfect association of SR chromosome inversions in present-day populations. Based on comparative genomic analyses, direct recombination experiments, segregation distortion assays, and population genetic modeling, we conclude the combined action of suppressed recombination and strong, ongoing, epistatic selection shape the D. pseudoobscura SR arrangement into a highly differentiated chromosome.
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34

KONDO, MARIKO, ERIKO NAGAO, HIROSHI MITANI, and AKIHIRO SHIMA. "Differences in recombination frequencies during female and male meioses of the sex chromosomes of the medaka, Oryzias latipes." Genetical Research 78, no. 1 (August 2001): 23–30. http://dx.doi.org/10.1017/s0016672301005109.

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In the medaka, Oryzias latipes, sex is determined chromosomally. The sex chromosomes differ from those of mammals in that the X and Y chromosomes are highly homologous. Using backcross panels for linkage analysis, we mapped 21 sequence tagged site (STS) markers on the sex chromosomes (linkage group 1). The genetic map of the sex chromosome was established using male and female meioses. The genetic length of the sex chromosome was shorter in male than in female meioses. The region where male recombination is suppressed is the region close to the sex-determining gene y, while female recombination was suppressed in both the telomeric regions. The restriction in recombination does not occur uniformly on the sex chromosome, as the genetic map distances of the markers are not proportional in male and female recombination. Thus, this observation seems to support the hypothesis that the heterogeneous sex chromosomes were derived from suppression of recombination between autosomal chromosomes. In two of the markers, Yc-2 and Casp6, which were expressed sequence-tagged (EST) sites, polymorphisms of both X and Y chromosomes were detected. The alleles of the X and Y chromosomes were also detected in O. curvinotus, a species related to the medaka. These markers could be used for genotyping the sex chromosomes in the medaka and other species, and could be used in other studies on sex chromosomes.
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35

BERSET-BRÄNDLI, L., J. JAQUIÉRY, and N. PERRIN. "Recombination is suppressed and variability reduced in a nascent Y chromosome." Journal of Evolutionary Biology 20, no. 3 (May 2007): 1182–88. http://dx.doi.org/10.1111/j.1420-9101.2006.01278.x.

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36

Hussain, Asif, Jianhua Hou, Muhammad Tahir, Xiaozhi Wang, Muhammad U. Qadri, Ting jiang, Xinyue Tu, Tingting Zhang, Qian Dou, and Ji-jun Zou. "Fine-tuning internal electric field of BiOBr for suppressed charge recombination." Journal of Environmental Chemical Engineering 9, no. 1 (February 2021): 104766. http://dx.doi.org/10.1016/j.jece.2020.104766.

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37

Willers, Henning, Ellen E. McCarthy, Petra Hubbe, Jochen Dahm-Daphi, and Simon N. Powell. "Homologous recombination in extrachromosomal plasmid substrates is not suppressed by p53." Carcinogenesis 22, no. 11 (November 2001): 1757–63. http://dx.doi.org/10.1093/carcin/22.11.1757.

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38

Kovalchuk, Olga, Carrie A. Hendricks, Scott Cassie, Andrew J. Engelward, and Bevin P. Engelward. "In vivo Recombination After Chronic Damage Exposure Falls to Below Spontaneous Levels in “Recombomice”." Molecular Cancer Research 2, no. 10 (October 1, 2004): 567–73. http://dx.doi.org/10.1158/1541-7786.567.2.10.

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Abstract All forms of cancer are initiated by heritable changes in gene expression. Although point mutations have been studied extensively, much less is known about homologous recombination events, despite its role in causing sequence rearrangements that contribute to tumorigenesis. Although transgenic mice that permit detection of point mutations have provided a fundamental tool for studying point mutations in vivo, until recently, transgenic mice designed specifically to detect homologous recombination events in somatic tissues in vivo did not exist. We therefore created fluorescent yellow direct repeat mice, enabling automated detection of recombinant cells in vivo for the first time. Here, we show that an acute dose of ionizing radiation induces recombination in fluorescent yellow direct repeat mice, providing some of the first direct evidence that ionizing radiation induces homologous recombination in cutaneous tissues in vivo. In contrast, the same total dose of radiation given under chronic exposure conditions suppresses recombination to levels that are significantly below those of unexposed animals. In addition, global methylation is suppressed and key DNA repair proteins are induced in tissues from chronically irradiated animals (specifically AP endonuclease, polymerase β, and Ku70). Thus, increased clearance of recombinogenic lesions may contribute to suppression of homologous recombination. Taken together, these studies show that fluorescent yellow direct repeat mice provide a rapid and powerful assay for studying the recombinogenic effects of both short-term and long-term exposure to DNA damage in vivo and reveal for the first time that exposure to ionizing radiation can have opposite effects on genomic stability depending on the duration of exposure.
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39

Erdeniz, Naz, and Rodney Rothstein. "Rsp5, a Ubiquitin-Protein Ligase, Is Involved in Degradation of the Single-Stranded-DNA Binding Protein Rfa1 inSaccharomyces cerevisiae." Molecular and Cellular Biology 20, no. 1 (January 1, 2000): 224–32. http://dx.doi.org/10.1128/mcb.20.1.224-232.2000.

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ABSTRACT In Saccharomyces cerevisiae, RAD1 andRAD52 are required for alternate pathways of mitotic recombination. Double-mutant strains exhibit a synergistic interaction that decreases direct repeat recombination rates dramatically. A mutation in RFA1, the largest subunit of a single-stranded DNA-binding protein complex (RP-A), suppresses the recombination deficiency of rad1 rad52 strains (J. Smith and R. Rothstein, Mol. Cell. Biol. 15:1632–1641, 1995). Previously, we hypothesized that this mutation, rfa1-D228Y, causes an increase in recombinogenic lesions as well as the activation of aRAD52-independent recombination pathway. To identify gene(s) acting in this pathway, temperature-sensitive (ts) mutations were screened for those that decrease recombination levels in arad1 rad52 rfa1-D228Y strain. Three mutants were isolated. Each segregates as a single recessive gene. Two are allelic toRSP5, which encodes an essential ubiquitin-protein ligase. One allele, rsp5-25, contains two mutations within its open reading frame. The first mutation does not alter the amino acid sequence of Rsp5, but it decreases the amount of full-length protein in vivo. The second mutation results in the substitution of a tryptophan with a leucine residue in the ubiquitination domain. Inrsp5-25 mutants, the UV sensitivity ofrfa1-D228Y is suppressed to the same level as in strains overexpressing Rfa1-D228Y. Measurement of the relative rate of protein turnover demonstrated that the half-life of Rfa1-D228Y inrsp5-25 mutants was extended to 65 min compared to a 35-min half-life in wild-type strains. We propose that Rsp5 is involved in the degradation of Rfa1 linking ubiquitination with the replication-recombination machinery.
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40

Charlesworth, Deborah. "Evolution of recombination rates between sex chromosomes." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1736 (November 6, 2017): 20160456. http://dx.doi.org/10.1098/rstb.2016.0456.

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In species with genetic sex-determination, the chromosomes carrying the sex-determining genes have often evolved non-recombining regions and subsequently evolved the full set of characteristics denoted by the term ‘sex chromosomes’. These include size differences, creating chromosomal heteromorphism, and loss of gene functions from one member of the chromosome pair. Such characteristics and changes have been widely reviewed, and underlie molecular genetic approaches that can detect sex chromosome regions. This review deals mainly with the evolution of new non-recombining regions, focusing on how certain evolutionary situations select for suppressed recombination (rather than the proximate mechanisms causing suppressed recombination between sex chromosomes). Particularly important is the likely involvement of sexually antagonistic polymorphisms in genome regions closely linked to sex-determining loci. These may be responsible for the evolutionary strata of sex chromosomes that have repeatedly formed by recombination suppression evolving across large genome regions. More studies of recently evolved non-recombining sex-determining regions should help to test this hypothesis empirically, and may provide evidence about whether other situations can sometimes lead to sex-linked regions evolving. Similarities with other non-recombining genome regions are discussed briefly, to illustrate common features of the different cases, though no general properties apply to all of them. This article is part of the themed issue ‘Evolutionary causes and consequences of recombination rate variation in sexual organisms’.
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41

Qu, Jie, Yongan Yang, Qingduan Wu, Paul R. Coxon, Yingjun Liu, Xiong He, Kai Xi, Ningyi Yuan, and Jianning Ding. "Hedgehog-like hierarchical ZnO needle-clusters with superior electron transfer kinetics for dye-sensitized solar cells." RSC Adv. 4, no. 22 (2014): 11430–37. http://dx.doi.org/10.1039/c3ra45929b.

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Owing to their unique morphology, hedgehog-like ZnO needle-clusters show enhanced photovoltaic conversion efficiencies and superior electron transfer kinetics: fast electron transfer and long lifetimes with suppressed recombination.
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42

Fu, Cen-Feng, Xingxing Li, and Jinlong Yang. "A rationally designed two-dimensional MoSe2/Ti2CO2 heterojunction for photocatalytic overall water splitting: simultaneously suppressing electron–hole recombination and photocorrosion." Chemical Science 12, no. 8 (2021): 2863–69. http://dx.doi.org/10.1039/d0sc06132h.

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The two challenges of electron–hole recombination and photocorrosion for two-dimensional transition metal dichalcogenides in the application of photocatalytic water splitting are simultaneously suppressed by rational design of heterojunctions.
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43

Luo, Liming, Jaesung Lee, and David L. Herrin. "Mapping of the css (chloroplast splicing suppressor) gene(s) to a recombinationally suppressed region of chromosome III in Chlamydomonas reinhardtii." Genome 55, no. 7 (July 2012): 483–91. http://dx.doi.org/10.1139/g2012-035.

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In previous work, three suppressors of defective group I introns (7151, 71N1, 7120) were isolated from a mutant of Chlamydomonas reinhardtii that had a splicing-deficient chloroplast large subunit (LSU) rRNA intron. Genetic analysis indicated that the 7151 and 71N1 suppressor mutations each involved single nuclear loci, and that the 7151 mutation was dominant. Here we present genetic evidence that the 7120 suppressor also involves a single nuclear locus and that the mutation is dominant in vegetative diploids. Moreover, we have employed crosses with the S1D2 strain and molecular markers to map the 7120 and 71N1 suppressors. Based on an analysis of 800 progeny from 7120 × S1D2, the 7120 suppressor is located in a region of ∼400 kb on chromosome III that is devoid of recombination. The ∼400-kb region contains at least 72 genes, about one-third of which (i.e., 22) are predicted to be organelle targeted. Similar analysis of 71N1 × S1D2 using 400 progeny also pointed to the recombination-deficient region of chromosome III, raising the possibility that these mutations could affect the same gene. These efforts lay the foundation for identifying the css (chloroplast splicing suppressor) gene(s), which promotes splicing of multiple chloroplast group I introns.
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44

Shor, Erika, Serge Gangloff, Marisa Wagner, Justin Weinstein, Gavrielle Price, and Rodney Rothstein. "Mutations in Homologous Recombination Genes Rescue top3 Slow Growth in Saccharomyces cerevisiae." Genetics 162, no. 2 (October 1, 2002): 647–62. http://dx.doi.org/10.1093/genetics/162.2.647.

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Abstract In budding yeast, loss of topoisomerase III, encoded by the TOP3 gene, leads to a genomic instability phenotype that includes slow growth, hyper-sensitivity to genotoxic agents, mitotic hyper-recombination, increased chromosome missegregation, and meiotic failure. Slow growth and other defects of top3 mutants are suppressed by mutation of SGS1, which encodes the only RecQ helicase in S. cerevisiae. sgs1 is epistatic to top3, suggesting that the two proteins act in the same pathway. To identify other factors that function in the Sgs1-Top3 pathway, we undertook a genetic screen for non-sgs1 suppressors of top3 defects. We found that slow growth and DNA damage sensitivity of top3 mutants are suppressed by mutations in RAD51, RAD54, RAD55, and RAD57. In contrast, top3 mutants show extreme synergistic growth defects with mutations in RAD50, MRE11, XRS2, RDH54, and RAD1. We also analyzed recombination at the SUP4-o region, showing that in a rad51, rad54, rad55, or rad57 background top3Δ does not increase recombination to the same degree as in a wild-type strain. These results suggest that the presence of the Rad51 homologous recombination complex in a top3 background facilitates creation of detrimental intermediates by Sgs1. We present a model wherein Rad51 helps recruit Sgs1-Top3 to sites of replicative damage.
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45

Li, Chun-Ting, Feng-Ling Wu, Chia-Jung Liang, Kuo-Chuan Ho, and Jiann T. Lin. "Effective suppression of interfacial charge recombination by a 12-crown-4 substituent on a double-anchored organic sensitizer and rotating disk electrochemical evidence." Journal of Materials Chemistry A 5, no. 16 (2017): 7586–94. http://dx.doi.org/10.1039/c6ta11091f.

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A crown-ether-substituted double-anchored organic dye suppressed charge recombination with iodide and cobalt redox mediators to reach the efficiencies of 10.12% (under 1 sun) and 11.17% (under 0.1 sun).
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46

Spell, Rachelle Miller, and Sue Jinks-Robertson. "Role of Mismatch Repair in the Fidelity ofRAD51- andRAD59-Dependent Recombination inSaccharomyces cerevisiae." Genetics 165, no. 4 (December 1, 2003): 1733–44. http://dx.doi.org/10.1093/genetics/165.4.1733.

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AbstractTo prevent genome instability, recombination between sequences that contain mismatches (homeologous recombination) is suppressed by the mismatch repair (MMR) pathway. To understand the interactions necessary for this regulation, the genetic requirements for the inhibition of homeologous recombination were examined using mutants in the RAD52 epistasis group of Saccharomyces cerevisiae. The use of a chromosomal inverted-repeat recombination assay to measure spontaneous recombination between 91 and 100% identical sequences demonstrated differences in the fidelity of recombination in pathways defined by their dependence on RAD51 and RAD59. In addition, the regulation of homeologous recombination in rad51 and rad59 mutants displayed distinct patterns of inhibition by different members of the MMR pathway. Whereas the requirements for the MutS homolog, MSH2, and the MutL homolog, MLH1, in the suppression of homeologous recombination were similar in rad51 strains, the loss of MSH2 caused a greater loss in homeologous recombination suppression than did the loss of MLH1 in a rad59 strain. The nonequivalence of the regulatory patterns in the wild-type and mutant strains suggests an overlap between the roles of the RAD51 and RAD59 gene products in potential cooperative recombination mechanisms used in wild-type cells.
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Klein, Hannah L. "Spontaneous Chromosome Loss in Saccharomyces cerevisiae Is Suppressed by DNA Damage Checkpoint Functions." Genetics 159, no. 4 (December 1, 2001): 1501–9. http://dx.doi.org/10.1093/genetics/159.4.1501.

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Abstract Genomic instability is one of the hallmarks of cancer cells and is often the causative factor in revealing recessive gene mutations that progress cells along the pathway to unregulated growth. Genomic instability can take many forms, including aneuploidy and changes in chromosome structure. Chromosome loss, loss and reduplication, and deletions are the majority events that result in loss of heterozygosity (LOH). Defective DNA replication, repair, and recombination can significantly increase the frequency of spontaneous genomic instability. Recently, DNA damage checkpoint functions that operate during the S-phase checkpoint have been shown to suppress spontaneous chromosome rearrangements in haploid yeast strains. To further study the role of DNA damage checkpoint functions in genomic stability, we have determined chromosome loss in DNA damage checkpoint-deficient yeast strains. We have found that the DNA damage checkpoints are essential for preserving the normal chromosome number and act synergistically with homologous recombination functions to ensure that chromosomes are segregated correctly to daughter cells. Failure of either of these processes increases LOH events. However, loss of the G2/M checkpoint does not result in an increase in chromosome loss, suggesting that it is the various S-phase DNA damage checkpoints that suppress chromosome loss. The mec1 checkpoint function mutant, defective in the yeast ATR homolog, results in increased recombination through a process that is distinct from that operative in wild-type cells.
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48

Yu, Juan, Wenran Wang, Zhenxiao Pan, Jun Du, Zhenwei Ren, Weinan Xue, and Xinhua Zhong. "Quantum dot sensitized solar cells with efficiency over 12% based on tetraethyl orthosilicate additive in polysulfide electrolyte." Journal of Materials Chemistry A 5, no. 27 (2017): 14124–33. http://dx.doi.org/10.1039/c7ta04344a.

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Benefiting from the suppressed charge recombination occurring at the photoanode/electrolyte interfaces with the introduction of TEOS additive in the polysulfide electrolyte, a remarkable PCE of over 12% was obtained for ZCISe QDSCs.
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49

Souza-Júnior, S. A., E. A. L. Gonçalves, S. A. Catanzaro-Guimarães, and M. A. A. Castro-Prado. "Loss of heterozygosity by mitotic recombination in diploid strain of Aspergillus nidulans in response to castor oil plant detergent." Brazilian Journal of Biology 64, no. 4 (November 2004): 885–90. http://dx.doi.org/10.1590/s1519-69842004000500019.

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Somatic recombination in heterozygous diploid cells may be a promotional agent of neoplasms by inducing homozygosity of defective genes. Tumor suppressor genes may in this way be completely suppressed in recombinant cells. In this work, the genotoxic effects of detergent derived from the castor oil plant (Ricinus communis) in heterozygous diploid cells of Aspergillus nidulans are evaluated. Previous studies have evaluated the application of this substance in endodontic treatments as an irrigating solution. The recombinogenic potential of the compound has been studied through the production of homozygous cells for nutritional markers riboA1, pabaA124, biA1, methA17, and pyroA4. Detergent was diluted to 1:10, 1:20, and 1:40, and morphologic alterations, delay in conidiophore development, and mitotic recombination occurrence were reported for the three dilutions. Although past studies have demonstrated the antimicrobial action of the detergent under analysis, our results revealed its cytotoxic effects and recombinogenic potential.
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50

Lim, Gyubum, Yeonji Chang, and Won-Ki Huh. "Phosphoregulation of Rad51/Rad52 by CDK1 functions as a molecular switch for cell cycle–specific activation of homologous recombination." Science Advances 6, no. 6 (February 2020): eaay2669. http://dx.doi.org/10.1126/sciadv.aay2669.

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Abstract:
Homologous recombination is exquisitely activated only during specific cell phases. In the G1 phase, homologous recombination activity is completely suppressed. According to previous reports, the activation of homologous recombination during specific cell phases depends on the kinase activity of cyclin-dependent kinase 1 (CDK1). However, the precise regulatory mechanism and target substrates of CDK1 for this regulation have not been completely determined. Here, we report that the budding yeast CDK1, Cdc28, phosphorylates the major homologous recombination regulators Rad51 and Rad52. This phosphorylation occurs in the G2/M phase by Cdc28 in combination with G2/M phase cyclins. Nonphosphorylatable mutations in Rad51 and Rad52 impair the DNA binding affinity of Rad51 and the affinity between Rad52 rings that leads to their interaction. Collectively, our data provide detailed insights into the regulatory mechanism of cell cycle–dependent homologous recombination activation in eukaryotic cells.
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