Journal articles on the topic 'Recombination'
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1
Persiani, D. M., J. Durdik, and E. Selsing. "Active lambda and kappa antibody gene rearrangement in Abelson murine leukemia virus-transformed pre-B cell lines." Journal of Experimental Medicine 165, no. 6 (June 1, 1987): 1655–74. http://dx.doi.org/10.1084/jem.165.6.1655.
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The two Abelson murine leukemia virus (A-MuLV)-transformed cell lines, BM18-4 and ABC-1, undergo immunoglobulin L-chain gene recombination during passage in tissue culture. BM18-4 cells are capable of kappa gene recombination, whereas ABC-1 cells are capable of both kappa and lambda gene recombination. The expression of H chains is apparently not necessary for continuing L chain gene recombination in either of these cells, although H-chain expression may have been involved in the initiation of L-chain gene recombination. All ABC-1 cells that have lambda gene rearrangements also display recombined kappa alleles, supporting the hypothesis that kappa and lambda gene recombination are initiated in an ordered, developmentally regulated manner in maturing B cells. However, analyses of the ABC-1 line indicate that pre-B cells that have initiated lambda gene recombination do not terminate kappa gene rearrangement. The lambda gene recombinations that occur in the ABC-1 cell line indicate that the germline order of lambda gene segments is: 5' ... V lambda 2 ... J lambda 2C lambda 2-J lambda 4C lambda 4 ... V lambda 1 ... J lambda 3C lambda 3-J lambda 1C lambda 1 ... 3'. In addition, the frequencies of lambda 1, lambda 2, and lambda 3 gene recombinations among ABC-1 cells are quite different than the frequencies of B cells producing lambda 1, lambda 2, and lambda 3 L-chains in the mouse. RS DNA recombinations also occur in the BM18-4 and ABC-1 cell lines, supporting the notion that Ig gene recombinases are involved in RS rearrangement. Recombined RS segments are infrequent among BM 18-4 cells but common among ABC-1 cells, suggesting that RS recombinational events often occur in maturing pre-B cells just before initiation of lambda gene rearrangements. This developmental timing is consistent with the hypothesis that RS recombination may be involved in the initiation of lambda gene assembly.
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STAUFFER, D., and S. CEBRAT. "EXTINCTION IN GENETIC BIT-STRING MODEL WITH SEXUAL RECOMBINATION." Advances in Complex Systems 09, no. 01n02 (March 2006): 147–56. http://dx.doi.org/10.1142/s0219525906000653.
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We have analyzed the relations between the mutational pressure, recombination and selection pressure in the bit-string model with sexual reproduction. For specific sets of these parameters, we have found three phase transitions with one phase where populations can survive. In this phase, recombination enhances the survival probability. Even if recombination is associated, to some extent, with additional mutations it could be advantageous to reproduction, indicating that the frequencies of recombinations and recombination-associated mutations can self-organize in Nature. Partitioning the diploid genome into pairs of chromosomes independently assorted during gamete production enables recombinations between groups of genes without the risk of mutations and is also advantageous for the strategy of sexual reproduction.
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Nebrin, Olof. "Case A or Case B? The Effective Recombination Coefficient in Gas Clouds of Arbitrary Optical Thickness." Research Notes of the AAS 7, no. 5 (May 10, 2023): 90. http://dx.doi.org/10.3847/2515-5172/acd37a.
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Abstract In calculations of the ionization state, one is often forced to choose between the Case A recombination coefficient α A (sum over recombinations to all hydrogen states) or the Case B recombination coefficient α B (sum over all hydrogen states except the ground state). If the cloud is optically thick to ionizing photons, α B is usually adopted on the basis of the “on-the-spot” approximation, wherein recombinations to the ground state are ignored because they produce ionizing photons absorbed nearby. In the opposite case of an optically thin cloud, one would expect the Case A recombination coefficient to better describe the effective recombination rate in the cloud. In this paper, I derive an analytical expression for the effective recombination coefficient in a gas cloud of arbitrary optical thickness which transitions from α A to α B as the optical thickness increases. The results can be readily implemented in numerical simulations and semi-analytical calculations.
4
Kuzminov, Andrei. "Recombinational Repair of DNA Damage inEscherichia coli and Bacteriophage λ." Microbiology and Molecular Biology Reviews 63, no. 4 (December 1, 1999): 751–813. http://dx.doi.org/10.1128/mmbr.63.4.751-813.1999.
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SUMMARY Although homologous recombination and DNA repair phenomena in bacteria were initially extensively studied without regard to any relationship between the two, it is now appreciated that DNA repair and homologous recombination are related through DNA replication. In Escherichia coli, two-strand DNA damage, generated mostly during replication on a template DNA containing one-strand damage, is repaired by recombination with a homologous intact duplex, usually the sister chromosome. The two major types of two-strand DNA lesions are channeled into two distinct pathways of recombinational repair: daughter-strand gaps are closed by the RecF pathway, while disintegrated replication forks are reestablished by the RecBCD pathway. The phage λ recombination system is simpler in that its major reaction is to link two double-stranded DNA ends by using overlapping homologous sequences. The remarkable progress in understanding the mechanisms of recombinational repair in E. coli over the last decade is due to the in vitro characterization of the activities of individual recombination proteins. Putting our knowledge about recombinational repair in the broader context of DNA replication will guide future experimentation.
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Myers, Simon R., and Robert C. Griffiths. "Bounds on the Minimum Number of Recombination Events in a Sample History." Genetics 163, no. 1 (January 1, 2003): 375–94. http://dx.doi.org/10.1093/genetics/163.1.375.
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Abstract Recombination is an important evolutionary factor in many organisms, including humans, and understanding its effects is an important task facing geneticists. Detecting past recombination events is thus important; this article introduces statistics that give a lower bound on the number of recombination events in the history of a sample, on the basis of the patterns of variation in the sample DNA. Such lower bounds are appropriate, since many recombination events in the history are typically undetectable, so the true number of historical recombinations is unobtainable. The statistics can be calculated quickly by computer and improve upon the earlier bound of Hudson and Kaplan (1985). A method is developed to combine bounds on local regions in the data to produce more powerful improved bounds. The method is flexible to different models of recombination occurrence. The approach gives recombination event bounds between all pairs of sites, to help identify regions with more detectable recombinations, and these bounds can be viewed graphically. Under coalescent simulations, there is a substantial improvement over the earlier method (of up to a factor of 2) in the expected number of recombination events detected by one of the new minima, across a wide range of parameter values. The method is applied to data from a region within the lipoprotein lipase gene and the amount of detected recombination is substantially increased. Further, there is strong clustering of detected recombination events in an area near the center of the region. A program implementing these statistics, which was used for this article, is available from http://www.stats.ox.ac.uk/mathgen/programs.html.
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Kleinfield, R. W., and M. G. Weigert. "Analysis of VH gene replacement events in a B cell lymphoma." Journal of Immunology 142, no. 12 (June 15, 1989): 4475–82. http://dx.doi.org/10.4049/jimmunol.142.12.4475.
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Abstract We have analyzed a series of recombinational events at the IgH chain locus of the B cell lymphoma, NFS-5. Each of these recombinational events results in the replacement of the VH gene segment of the rearranged H chain gene (VhDJh) with that of an upstream germline gene segment. Replacements on the productive and nonproductive alleles have been observed. In each case, the recombination occurs in close proximity to a highly conserved heptameric sequence (5'TACTGTG3') which is located at the 3' end of the VH coding region. In the two examples of recombination on the productive allele that have been analyzed, the initial VHQ52 gene is replaced by different VH7183 genes. On the non-productive allele, sequential replacement events have been analyzed: the initial VHQ52 rearrangement is first replaced by a closely related VHQ52 gene, followed by a second replacement using a VHQ52 pseudogene. Southern blot analysis using VH probes indicates that these recombinations may be accompanied by the deletion of germline VH genes belonging to both the VHQ52 and VH7183 families, suggesting that these gene families are interspersed in the NFS/N mouse.
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CERBANIC, GEORGETA, IOAN BURDA, and SIMION SIMON. "RECOMBINATION PARAMETERS OF CdxI1-xSe EPITAXIAL LAYERS FROM THE PHOTOCONDUCTIVE EFFECT." Modern Physics Letters B 15, no. 27 (November 20, 2001): 1225–30. http://dx.doi.org/10.1142/s0217984901003135.
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The study of lifetimes regarding the recombination of non-equilibrium carriers and their kinetics is essential in order to explain the recombination mechanisms in semiconductors. The study of recombination kinetics and lifetime values in CdSe epitaxial layers is the target of this paper. CdSe layers have been deposited on (0001) mica substrates by vapor epitaxial method. The epitaxial layers contain defects that induce gap states and specific recombination kinetics. The lifetimes were determined by photoconductive frequency-resolved spectroscopy (PCFRS), a usual method for such measurements. The lifetime spectra obtained show in all studied samples the presence of three types of recombinations: τ1 is due to band-to-band recombination, τ2 to surface recombination associated with chemical impurities and τ3 to surface recombination associated with structural defects. The lifetime measured as a function of the substrate temperature denotes a complex correlation between the crystal perfection and the growth temperature.
8
Petrini, J., and W. A. Dunnick. "Products and implied mechanism of H chain switch recombination." Journal of Immunology 142, no. 8 (April 15, 1989): 2932–35. http://dx.doi.org/10.4049/jimmunol.142.8.2932.
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Abstract The Ig H chain switch is a DNA recombination event. The recombination occurs between two or more switch regions, areas of tandem sequence duplication that lie upstream of the corresponding H chain C region genes. We have determined the DNA sequence at four recombination sites in three molecularly cloned, rearranged switch regions. All eight donor and recipient recombination sites are at the common pentamers GGGGT, GAGCT, and GGTGG. One of the switch recombination events is an inversion of S gamma 3 sequences. Another of the recombinational events is an internal S gamma 1 deletion, which may be switch enzyme mediated. These results, together with other switch recombination site sequences, suggest that switch recombination is mediated by cutting enzymes with modest specificity and religation enzymes with no specificity.
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Li, Ting, and Jiayou Zhang. "Intramolecular Recombinations of Moloney Murine Leukemia Virus Occur during Minus-Strand DNA Synthesis." Journal of Virology 76, no. 19 (October 1, 2002): 9614–23. http://dx.doi.org/10.1128/jvi.76.19.9614-9623.2002.
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ABSTRACT Retroviral recombination can occur between two viral RNA molecules (intermolecular) or between two sequences within the same RNA molecule (intramolecular). The rate of retroviral intramolecular recombination is high. Previous studies showed that, after a single round of replication, 50 to 60% of retroviral recombinations occur between two identical sequences within a Moloney murine leukemia virus-based vector. Recombination can occur at any polymerization step within the retroviral replication cycle. Although reverse transcriptase is assumed to contribute to the template switches, previous studies could not distinguish between changes introduced by host RNA polymerase II (Pol II) or by reverse transcriptase. A cell culture system has been established to detect the individual contribution of host RNA Pol II, host DNA polymerase or viral reverse transcriptase, as well as the recombination events taking place during minus-strand DNA synthesis and plus-strand DNA synthesis in a single round of viral intramolecular replication. Studies in this report demonstrate that intramolecular recombination between two identical sequences during transcription by host RNA Pol II is minimal and that most recombinations occur during minus-strand DNA synthesis catalyzed by viral reverse transcriptase.
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Coutinho, Thamara Carvalho, Telles Timóteo Da Silva, and Gustavo Leal Toledo. "Recombination and Genetic Diversity." TEMA (São Carlos) 13, no. 3 (December 22, 2012): 265–75. http://dx.doi.org/10.5540/tema.2013.013.03.0265.
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In this paper we present a spatial stochastic model for genetic recombination, that answers if diversity is preserved in an infinite population of recombinating individuals distributed spatially. We show that, for finite times, recombination may maintain all the various potential different types, but when time grows infinitely, the diversity of individuals extinguishes off. So under the model premisses, recombination and spatial localization alone are not enough to explain diversity in a population. Further we discuss an application of the model to a controversy regarding the diversity of "Major Histocompatibility Complex" (MHC).
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Halbrook, J., and M. F. Hoekstra. "Mutations in the Saccharomyces cerevisiae CDC1 gene affect double-strand-break-induced intrachromosomal recombination." Molecular and Cellular Biology 14, no. 12 (December 1994): 8037–50. http://dx.doi.org/10.1128/mcb.14.12.8037-8050.1994.
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To isolate Saccharomyces cerevisiae mutants defective in recombinational DNA repair, we constructed a strain that contains duplicated ura3 alleles that flank LEU2 and ADE5 genes at the ura3 locus on chromosome V. When a HO endonuclease cleavage site is located within one of the ura3 alleles, Ura+ recombination is increased over 100-fold in wild-type strains following HO induction from the GAL1, 10 promoter. This strain was used to screen for mutants that exhibited reduced levels of HO-induced intrachromosomal recombination without significantly affecting the spontaneous frequency of Ura+ recombination. One of the mutations isolated through this screen was found to affect the essential gene CDC1. This mutation, cdc1-100, completely eliminated HO-induced Ura+ recombination yet maintained both spontaneous preinduced recombination levels and cell viability, cdc1-100 mutants were moderately sensitive to killing by methyl methanesulfonate and gamma irradiation. The effect of the cdc1-100 mutation on recombinational double-strand break repair indicates that a recombinationally silent mechanism other than sister chromatid exchange was responsible for the efficient repair of DNA double-strand breaks.
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Katzourakis, Aris, Vini Pereira, and Michael Tristem. "Effects of Recombination Rate on Human Endogenous Retrovirus Fixation and Persistence." Journal of Virology 81, no. 19 (July 18, 2007): 10712–17. http://dx.doi.org/10.1128/jvi.00410-07.
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ABSTRACT Endogenous retroviruses (ERVs) result from germ line infections by exogenous retroviruses. They can proliferate within the genome of their host species until they are either inactivated by mutation or removed by recombinational deletion. ERVs belong to a diverse group of mobile genetic elements collectively termed transposable elements (TEs). Numerous studies have attempted to elucidate the factors determining the genomic distribution and persistence of TEs. Here we show that, within humans, gene density and not recombination rate correlates with fixation of endogenous retroviruses, whereas the local recombination rate determines their persistence in a full-length state. Recombination does not appear to influence fixation either via the ectopic exchange model or by indirect models based on the efficacy of selection. We propose a model linking rates of meiotic recombination to the probability of recombinational deletion to explain the effect of recombination rate on persistence. Chromosomes 19 and Y are exceptions, possessing more elements than other regions, and we suggest this is due to low gene density and elevated rates of human ERV integration in males for chromosome Y and segmental duplication for chromosome 19.
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Halbrook, J., and M. F. Hoekstra. "Mutations in the Saccharomyces cerevisiae CDC1 gene affect double-strand-break-induced intrachromosomal recombination." Molecular and Cellular Biology 14, no. 12 (December 1994): 8037–50. http://dx.doi.org/10.1128/mcb.14.12.8037.
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To isolate Saccharomyces cerevisiae mutants defective in recombinational DNA repair, we constructed a strain that contains duplicated ura3 alleles that flank LEU2 and ADE5 genes at the ura3 locus on chromosome V. When a HO endonuclease cleavage site is located within one of the ura3 alleles, Ura+ recombination is increased over 100-fold in wild-type strains following HO induction from the GAL1, 10 promoter. This strain was used to screen for mutants that exhibited reduced levels of HO-induced intrachromosomal recombination without significantly affecting the spontaneous frequency of Ura+ recombination. One of the mutations isolated through this screen was found to affect the essential gene CDC1. This mutation, cdc1-100, completely eliminated HO-induced Ura+ recombination yet maintained both spontaneous preinduced recombination levels and cell viability, cdc1-100 mutants were moderately sensitive to killing by methyl methanesulfonate and gamma irradiation. The effect of the cdc1-100 mutation on recombinational double-strand break repair indicates that a recombinationally silent mechanism other than sister chromatid exchange was responsible for the efficient repair of DNA double-strand breaks.
14
Aylon, Yael, Batia Liefshitz, Gili Bitan-Banin, and Martin Kupiec. "Molecular Dissection of Mitotic Recombination in the Yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 23, no. 4 (February 15, 2003): 1403–17. http://dx.doi.org/10.1128/mcb.23.4.1403-1417.2003.
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ABSTRACT Recombination plays a central role in the repair of broken chromosomes in all eukaryotes. We carried out a systematic study of mitotic recombination. Using several assays, we established the chronological sequence of events necessary to repair a single double-strand break. Once a chromosome is broken, yeast cells become immediately committed to recombinational repair. Recombination is completed within an hour and exhibits two kinetic gaps. By using this kinetic framework we also characterized the role played by several proteins in the recombinational process. In the absence of Rad52, the broken chromosome ends, both 5′ and 3′, are rapidly degraded. This is not due to the inability to recombine, since the 3′ single-stranded DNA ends are stable in a strain lacking donor sequences. Rad57 is required for two consecutive strand exchange reactions. Surprisingly, we found that the Srs2 helicase also plays an early positive role in the recombination process.
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Zahradka, Davor, Ksenija Zahradka, Mirjana Petranović, Damir Đermić, and Krunoslav Brčić-Kostić. "The RuvABC Resolvase Is Indispensable for Recombinational Repair in sbcB15 Mutants of Escherichia coli." Journal of Bacteriology 184, no. 15 (August 1, 2002): 4141–47. http://dx.doi.org/10.1128/jb.184.15.4141-4147.2002.
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ABSTRACT The RuvABC proteins of Escherichia coli play an important role in the processing of Holliday junctions during homologous recombination and recombinational repair. Mutations in the ruv genes have a moderate effect on recombination and repair in wild-type strains but confer pronounced recombination deficiency and extreme sensitivity to DNA-damaging agents in a recBC sbcBC background. Genetic analysis presented in this work revealed that the ΔruvABC mutation causes an identical DNA repair defect in UV-irradiated recBC sbcBC, sbcBC, and sbcB strains, indicating that the sbcB mutation alone is responsible for the extreme UV sensitivity of recBC sbcBC ruv derivatives. In experiments with gamma irradiation and in conjugational crosses, however, sbcBC ΔruvABC and sbcB ΔruvABC mutants displayed higher recombination proficiency than the recBC sbcBC ΔruvABC strain. The frequency of conjugational recombination observed with the sbcB ΔruvABC strain was quite similar to that of the ΔruvABC single mutant, indicating that the sbcB mutation does not increase the requirement for RuvABC in a recombinational process starting from preexisting DNA ends. The differences between the results obtained in three experimental systems used suggest that in UV-irradiated cells, the RuvABC complex might act in an early stage of recombinational repair. The results of this work are discussed in the context of recent recombination models which propose the participation of RuvABC proteins in the processing of Holliday junctions made from stalled replication forks. We suggest that the mutant SbcB protein stabilizes these junctions and makes their processing highly dependent on RuvABC resolvase.
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Ivančić-Baće, Ivana, Erika Salaj-Šmic, and Krunoslav Brčić-Kostić. "Effects of recJ, recQ, and recFOR Mutations on Recombination in Nuclease-Deficient recB recD Double Mutants of Escherichia coli." Journal of Bacteriology 187, no. 4 (February 15, 2005): 1350–56. http://dx.doi.org/10.1128/jb.187.4.1350-1356.2005.
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ABSTRACT The two main recombination pathways in Escherichia coli (RecBCD and RecF) have different recombination machineries that act independently in the initiation of recombination. Three essential enzymatic activities are required for early recombinational processing of double-stranded DNA ends and breaks: a helicase, a 5′→3′ exonuclease, and loading of RecA protein onto single-stranded DNA tails. The RecBCD enzyme performs all of these activities, whereas the recombination machinery of the RecF pathway consists of RecQ (helicase), RecJ (5′→3′ exonuclease), and RecFOR (RecA-single-stranded DNA filament formation). The recombination pathway operating in recB (nuclease-deficient) mutants is a hybrid because it includes elements of both the RecBCD and RecF recombination machineries. In this study, genetic analysis of recombination in a recB (nuclease-deficient) recD double mutant was performed. We show that conjugational recombination and DNA repair after UV and gamma irradiation in this mutant are highly dependent on recJ, partially dependent on recFOR, and independent of recQ. These results suggest that the recombination pathway operating in a nuclease-deficient recB recD double mutant is also a hybrid. We propose that the helicase and RecA loading activities belong to the RecBCD recombination machinery, while the RecJ-mediated 5′→3′ exonuclease is an element of the RecF recombination machinery.
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Leung, H., and N. Maizels. "Regulation and targeting of recombination in extrachromosomal substrates carrying immunoglobulin switch region sequences." Molecular and Cellular Biology 14, no. 2 (February 1994): 1450–58. http://dx.doi.org/10.1128/mcb.14.2.1450-1458.1994.
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We have used extrachromosomal substrates carrying immunoglobulin heavy-chain S mu and S gamma 3 switch region sequences to study activation and targeting of recombination by a transcriptional enhancer element. Substrates are transiently introduced into activated primary murine B cells, in which recombination involving S-region sequences deletes a conditionally lethal marker, and recombination is measured by transformation of Escherichia coli in the second step of the assay. Previously we found that as many as 25% of replicated substrates recombined during 40-h transfection of lipopolysaccharide (LPS)-stimulated primary cells and that efficient recombination was dependent on the presence of S-region sequences as well as a transcriptional activator region in the constructs (H. Leung and N. Maizels, Proc. Natl. Acad. Sci. USA 89:4154-4158, 1992). Here we show that recombination of the switch substrates is threefold more efficient in LPS-cultured primary B cells than in the T-cell line EL4; the activities responsible for switch substrate recombination thus appear to be more abundant or more active in cells which can carry out chromosomal switch recombination. We test the role of the transcriptional activator region and show that the immunoglobulin heavy-chain intron enhancer (E mu) alone stimulates recombination as well as E mu combined with a heavy-chain promoter and that mutations that diminish enhancer-dependent transcription 500-fold diminish recombinational activation less than 2-fold. These observations suggest that the enhancer stimulates recombination by a mechanism that does not depend on transcript production or that is insensitive to the level of transcript production over a very broad range. Furthermore, we find that E mu stimulates recombination when located either upstream or downstream of S mu but that the position of the recombinational activator does affect the targeting of recombination junctions, suggesting that the relatively imprecise targeting of switch junctions in vivo may reflect the availability of many potential activator sites within each switch region.
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Leung, H., and N. Maizels. "Regulation and targeting of recombination in extrachromosomal substrates carrying immunoglobulin switch region sequences." Molecular and Cellular Biology 14, no. 2 (February 1994): 1450–58. http://dx.doi.org/10.1128/mcb.14.2.1450.
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We have used extrachromosomal substrates carrying immunoglobulin heavy-chain S mu and S gamma 3 switch region sequences to study activation and targeting of recombination by a transcriptional enhancer element. Substrates are transiently introduced into activated primary murine B cells, in which recombination involving S-region sequences deletes a conditionally lethal marker, and recombination is measured by transformation of Escherichia coli in the second step of the assay. Previously we found that as many as 25% of replicated substrates recombined during 40-h transfection of lipopolysaccharide (LPS)-stimulated primary cells and that efficient recombination was dependent on the presence of S-region sequences as well as a transcriptional activator region in the constructs (H. Leung and N. Maizels, Proc. Natl. Acad. Sci. USA 89:4154-4158, 1992). Here we show that recombination of the switch substrates is threefold more efficient in LPS-cultured primary B cells than in the T-cell line EL4; the activities responsible for switch substrate recombination thus appear to be more abundant or more active in cells which can carry out chromosomal switch recombination. We test the role of the transcriptional activator region and show that the immunoglobulin heavy-chain intron enhancer (E mu) alone stimulates recombination as well as E mu combined with a heavy-chain promoter and that mutations that diminish enhancer-dependent transcription 500-fold diminish recombinational activation less than 2-fold. These observations suggest that the enhancer stimulates recombination by a mechanism that does not depend on transcript production or that is insensitive to the level of transcript production over a very broad range. Furthermore, we find that E mu stimulates recombination when located either upstream or downstream of S mu but that the position of the recombinational activator does affect the targeting of recombination junctions, suggesting that the relatively imprecise targeting of switch junctions in vivo may reflect the availability of many potential activator sites within each switch region.
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Daitch, L. E., M. W. Moore, D. M. Persiani, J. M. Durdik, and E. Selsing. "Transcription and recombination of the murine RS element." Journal of Immunology 149, no. 3 (August 1, 1992): 832–40. http://dx.doi.org/10.4049/jimmunol.149.3.832.
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Abstract The deletion of C kappa is a frequent event in lambda-producing B cells in both mice and humans. Deletions of the murine C kappa gene are mediated by recombination events that involve the RS (recombining segment) element located downstream of the C kappa gene. RS recombinations appear to be mediated by the same mechanisms involved in Ig and TCR gene rearrangement. It has been suggested that RS recombinations might activate a factor that is involved in the initiation of lambda gene rearrangement in maturing pre-B cells. We have identified a unique RNA transcript derived from the recombined RS element present in some pre-B cell lines. However, gene transfer studies indicate that this RS transcript is not sufficient to induce lambda gene recombination in pre-B cell lines. We also find that recombination of the RS element in pre-B cell lines is closely correlated with changes in chromatin structure and transcriptional activation. Thus, recombination of the RS element in pre-B cells appears to be regulated in a manner similar to the regulation of antibody gene VDJ joining.
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Subramani, S., and J. Rubnitz. "Recombination events after transient infection and stable integration of DNA into mouse cells." Molecular and Cellular Biology 5, no. 4 (April 1985): 659–66. http://dx.doi.org/10.1128/mcb.5.4.659-666.1985.
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To investigate the recombinational machinery of mammalian cells, we have constructed plasmids that can be used as substrates for homologous recombination. These plasmids contain two truncated nontandem, but overlapping, segments of the neomycin resistance gene, separated by the transcription unit for the xanthine guanine phosphoribosyl transferase gene. Recombination between the two nonfunctional neomycin gene sequences generates an intact neomycin resistance gene that is functional in both bacteria and mammalian cells. Using these plasmid substrates, we have characterized the frequencies and products of recombination events that occur in mouse 3T6 cells soon after transfection and also after stable integration of these DNAs. Among the chromosomal recombination events, we have characterized apparent deletion events that can be accounted for by intrachromatid recombination or unequal sister chromatid exchanges. Other recombination events like chromosomal inversions and possible gene conversion events in an amplification unit are also described.
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Subramani, S., and J. Rubnitz. "Recombination events after transient infection and stable integration of DNA into mouse cells." Molecular and Cellular Biology 5, no. 4 (April 1985): 659–66. http://dx.doi.org/10.1128/mcb.5.4.659.
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To investigate the recombinational machinery of mammalian cells, we have constructed plasmids that can be used as substrates for homologous recombination. These plasmids contain two truncated nontandem, but overlapping, segments of the neomycin resistance gene, separated by the transcription unit for the xanthine guanine phosphoribosyl transferase gene. Recombination between the two nonfunctional neomycin gene sequences generates an intact neomycin resistance gene that is functional in both bacteria and mammalian cells. Using these plasmid substrates, we have characterized the frequencies and products of recombination events that occur in mouse 3T6 cells soon after transfection and also after stable integration of these DNAs. Among the chromosomal recombination events, we have characterized apparent deletion events that can be accounted for by intrachromatid recombination or unequal sister chromatid exchanges. Other recombination events like chromosomal inversions and possible gene conversion events in an amplification unit are also described.
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Ballantyne, Jack, Diane L. Henry, Jurgen R. Muller, Francine Briere, Clifford M. Snapper, Marilyn Kehry, and Kenneth B. Marcu. "Efficient Recombination of a Switch Substrate Retrovector in CD40-Activated B Lymphocytes: Implications for the Control of CH Gene Switch Recombination." Journal of Immunology 161, no. 3 (August 1, 1998): 1336–47. http://dx.doi.org/10.4049/jimmunol.161.3.1336.
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Abstract Maturing B lymphocytes possess a recombination activity that switches the class of heavy chain Ig. The nature of the recombination activity, its molecular requirements and regulation remain elusive questions about B lymphocyte biology and development. Class switch recombination is controlled by cytokine response elements that are required to differentially activate CH gene transcription before their subsequent recombination. Here, we show that cultures of purified murine and human B cells, stimulated only by CD40 receptor engagement, possess a potent switch recombination activity. CD40 ligand-stimulated murine and human B lymphocytes were infected with recombinant retroviruses containing Sμ and Sγ2b sequences. Chromosomally integrated switch substrate retrovectors (SSRs), harboring constitutively transcribed S sequences, underwent extensive recombinations restricted to their S sequences with structural features akin to endogenous switching. SSR recombination commenced 4 days postinfection (5 days poststimulation) with extensive switch sequence recombination over the next 2 to 3 days. In contrast, endogenous Sγ2b and Sγ1 sequences did not undergo appreciable switch recombination upon CD40 signaling alone. As expected, IL-4 induced endogenous Sμ to Sγ1 switching, while endogenous Sμ to Sγ2b fusions remained undetectable. Surprisingly, IL-4 enhanced the onset of SSR recombination in CD40-stimulated murine B cells, with S-S products appearing only 2 days postinfection and reaching a maximum within 2 to 3 days. The efficiency of switch recombination with SSRs ressembles that seen for endogenous CH class switching.
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Saparbaev, Murat, Louise Prakash, and Satya Prakash. "Requirement of Mismatch Repair Genes MSH2 and MSH3 in the RAD1-RAD10 Pathway of Mitotic Recombination in Saccharomyces cerevisiae." Genetics 142, no. 3 (March 1, 1996): 727–36. http://dx.doi.org/10.1093/genetics/142.3.727.
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Abstract The RAD1 and RAD10 genes of Saccharomyces cerevisiae are required for nucleotide excision repair and they also act in mitotic recombination. The Rad1-Rad10 complex has a single-stranded DNA endonuclease activity. Here, we show that the mismatch repair genes MSH2 and MSH3 function in mitotic recombination. For both his3 and his4 duplications, and for homologous integration of a linear DNA fragment into the genome, the msh3Δ mutation has an effect on recombination similar to that of the rad1Δ and rad10Δ mutations. The msh2Δ mutation also reduces the rate of recombination of the his3 duplication and lowers the incidence of homologous integration of a linear DNA fragment. Epistasis analyses indicate that MSH2 and MSH3 function in the RAD1-RAD10 recombination pathway, and studies presented here suggest an involvement of the RAD1-RAD10 pathway in reciprocal recombination. The possible roles of Msh2, Msh3, Rad1, and Rad10 proteins in genetic recombination are discussed. Coupling of mismatch binding proteins with the recombinational machinery could be important for ensuring genetic fidelity in the recombination process.
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Owens, J. D., F. D. Finkelman, J. D. Mountz, and J. F. Mushinski. "Nonhomologous recombination at sites within the mouse JH-C delta locus accompanies C mu deletion and switch to immunoglobulin D secretion." Molecular and Cellular Biology 11, no. 11 (November 1991): 5660–70. http://dx.doi.org/10.1128/mcb.11.11.5660-5670.1991.
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Plasma cells secrete immunoglobulins other than immunoglobulin M (IgM) after a deletion and recombination in which a portion of the immunoglobulin heavy-chain locus (IgH), from the 5'-flanking region of the mu constant-region gene (C mu) to the 5'-flanking region of the secreted heavy-chain constant-region gene (CH), is deleted. The recombination step is believed to be targeted via switch regions, stretches of repetitive DNA which lie in the 5' flank of all CH genes except delta. Although serum levels of IgD are very low, particularly in the mouse, IgD-secreting plasmacytomas of BALB/c and C57BL/6 mice are known. In an earlier study of two BALB/c IgD-secreting hybridomas, we reported that both had deleted the C mu gene, and we concluded that this deletion was common in the normal generation of IgD-secreting cells. To learn how such switch recombinations occur in the absence of a switch region upstream of the C delta 1 exon, we isolated seven more BALB/c and two C57BL/6 IgD-secreting hybridomas. We determined the DNA sequences of the switch recombination junctions in eight of these hybridomas as well as that of the C57BL/6 hybridoma B1-8. delta 1 and of the BALB/c, IgD-secreting plasmacytoma TEPC 1033. All of the lines had deleted the C mu gene, and three had deleted the C delta 1 exon in the switch recombination event. The delta switch recombination junction sequences were similar to those of published productive switch recombinations occurring 5' to other heavy-chain genes, suggesting that nonhomologous, illegitimate recombination is utilized whenever the heavy-chain switch region is involved in recombination.
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Owens, J. D., F. D. Finkelman, J. D. Mountz, and J. F. Mushinski. "Nonhomologous recombination at sites within the mouse JH-C delta locus accompanies C mu deletion and switch to immunoglobulin D secretion." Molecular and Cellular Biology 11, no. 11 (November 1991): 5660–70. http://dx.doi.org/10.1128/mcb.11.11.5660.
Full textAbstract:
Plasma cells secrete immunoglobulins other than immunoglobulin M (IgM) after a deletion and recombination in which a portion of the immunoglobulin heavy-chain locus (IgH), from the 5'-flanking region of the mu constant-region gene (C mu) to the 5'-flanking region of the secreted heavy-chain constant-region gene (CH), is deleted. The recombination step is believed to be targeted via switch regions, stretches of repetitive DNA which lie in the 5' flank of all CH genes except delta. Although serum levels of IgD are very low, particularly in the mouse, IgD-secreting plasmacytomas of BALB/c and C57BL/6 mice are known. In an earlier study of two BALB/c IgD-secreting hybridomas, we reported that both had deleted the C mu gene, and we concluded that this deletion was common in the normal generation of IgD-secreting cells. To learn how such switch recombinations occur in the absence of a switch region upstream of the C delta 1 exon, we isolated seven more BALB/c and two C57BL/6 IgD-secreting hybridomas. We determined the DNA sequences of the switch recombination junctions in eight of these hybridomas as well as that of the C57BL/6 hybridoma B1-8. delta 1 and of the BALB/c, IgD-secreting plasmacytoma TEPC 1033. All of the lines had deleted the C mu gene, and three had deleted the C delta 1 exon in the switch recombination event. The delta switch recombination junction sequences were similar to those of published productive switch recombinations occurring 5' to other heavy-chain genes, suggesting that nonhomologous, illegitimate recombination is utilized whenever the heavy-chain switch region is involved in recombination.
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Uchida, Tetsuya, Mariko Miyawaki, and Haruyasu Kinashi. "Chromosomal Arm Replacement in Streptomyces griseus." Journal of Bacteriology 185, no. 3 (February 1, 2003): 1120–24. http://dx.doi.org/10.1128/jb.185.3.1120-1124.2003.
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ABSTRACT UV irradiation of Streptomyces griseus 2247 yielded a new chromosomal deletion mutant, MM9. Restriction and sequencing analysis revealed that homologous recombination between two similar lipoprotein-like open reading frames, which are located 450 and 250 kb from the left and right ends, respectively, caused chromosomal arm replacement. As a result, new 450-kb terminal inverted repeats (TIRs) were formed in place of the original 24-kb TIRs. Frequent homologous recombinations in Streptomyces strains suggest that telomere deletions can usually be repaired by recombinational DNA repair functioning between the intact and deleted TIR sequences on the same chromosome.
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Fernex, C., M. Capone, and P. Ferrier. "The V(D)J recombinational and transcriptional activities of the immunoglobulin heavy-chain intronic enhancer can be mediated through distinct protein-binding sites in a transgenic substrate." Molecular and Cellular Biology 15, no. 6 (June 1995): 3217–26. http://dx.doi.org/10.1128/mcb.15.6.3217.
Full textAbstract:
Immunoglobulin and T-cell receptor gene transcriptional enhancers encompass sequences which stimulate V(D)J recombination of associated variable gene segments. To address the question of whether enhancer-mediated transcriptional activation and recombinational activation depend on the same cis-regulatory sequences, we have produced transgenic mice by using recombination substrates containing various mutations in the immunoglobulin heavy-chain intronic enhancer (E mu). Analysis of substrate rearrangements indicated that specific compound elements including E-box transcriptional motifs are crucial for the recombinational activity of E mu in the developing B and T lymphocytes. In most cases, a faithful correlation between the levels of substrate germ line transcription and recombination was observed. However, some of the E mu mutants which were able to activate transcription of the unrearranged substrate were inefficient in stimulating transgene recombination, implying that the latter function depends on molecular events other than the mere activation of transcription and that both activities can be mediated through distinct regulatory sequences. Together, these results support a model in which lymphoid gene enhancers, in addition to providing docking sites for factors that dictate transcriptional accessibility, must have some specific function(s) for activating V(D)J recombination.
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Niu, Yunwei, Xiaoxin Sun, Zuobing Xiao, Pinpin Wang, and Ruolin Wang. "Olfactory Impact of Terpene Alcohol on Terpenes Aroma Expression in Chrysanthemum Essential Oils." Molecules 23, no. 11 (October 29, 2018): 2803. http://dx.doi.org/10.3390/molecules23112803.
Full textAbstract:
The key point of our work was evaluating the impact of terpene alcohols on the aroma expression of terpenes recombination in Chrysanthemum essential oils. Using pure commercial products, various aromatic recombinations were prepared, consisting of terpenes recombination and six terpene alcohols, all the concentrations found in Chrysanthemum essential oils. There were five groups of terpene alcohols mixtures performed very interesting with the addition or omission tests. The “olfactory threshold” of the terpenes recombination had a notable decrease when adding isoborneol, d-Fenchyl alcohol respectively through the Feller’s additive model analysis. Furthermore, the descriptive test indicated that the addition of terpene alcohols mixture had the different effect on fruity, floral, woody, green, and herbal aroma intensity. Specifically, when isoborneol was added to the terpenes recombination in squalane solution, it was revealed that isoborneol had a synergy impact on herbal and green notes of the terpenes recombination and masked the fruity note.
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Oudinet, Chloé, Fatima-Zohra Braikia, Audrey Dauba, and Ahmed Amine Khamlichi. "Recombination may occur in the absence of transcription in the immunoglobulin heavy chain recombination centre." Nucleic Acids Research 48, no. 7 (February 22, 2020): 3553–66. http://dx.doi.org/10.1093/nar/gkaa108.
Full textAbstract:
Abstract Developing B cells undergo V(D)J recombination to generate a vast repertoire of Ig molecules. V(D)J recombination is initiated by the RAG1/RAG2 complex in recombination centres (RCs), where gene segments become accessible to the complex. Whether transcription is the causal factor of accessibility or whether it is a side product of other processes that generate accessibility remains a controversial issue. At the IgH locus, V(D)J recombination is controlled by Eμ enhancer, which directs the transcriptional, epigenetic and recombinational events in the IgH RC. Deletion of Eμ enhancer affects both transcription and recombination, making it difficult to conclude if Eμ controls the two processes through the same or different mechanisms. By using a mouse line carrying a CpG-rich sequence upstream of Eμ enhancer and analyzing transcription and recombination at the single-cell level, we found that recombination could occur in the RC in the absence of detectable transcription, suggesting that Eμ controls transcription and recombination through distinct mechanisms. Moreover, while the normally Eμ-dependent transcription and demethylating activities were impaired, recruitment of chromatin remodeling complexes was unaffected. RAG1 was efficiently recruited, thus compensating for the defective transcription-associated recruitment of RAG2, and providing a mechanistic basis for RAG1/RAG2 assembly to initiate V(D)J recombination.
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Nickoloff, J. A., and R. J. Reynolds. "Transcription stimulates homologous recombination in mammalian cells." Molecular and Cellular Biology 10, no. 9 (September 1990): 4837–45. http://dx.doi.org/10.1128/mcb.10.9.4837-4845.1990.
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Transcription stimulates homologous recombination in Saccharomyces cerevisiae and has been implicated in the control of recombinational events during the development of mammalian immune systems. Here, we describe a plasmid-based system in which an inducible promoter from the mouse mammary tumor virus is located upstream of heteroallelic neomycin genes carried on two plasmids. Pairs of plasmids are introduced into Chinese hamster ovary cells by electroporation, and recombination is monitored by scoring colonies resistant to the aminoglycoside G418. When transcription is induced with dexamethasone, a synthetic glucocorticoid hormone, and double-strand breaks are introduced at mutation sites, recombination is stimulated sixfold over noninduced levels. Inducing transcription in circular substrates or in substrates cleaved at sites distant from the mutations has no detectable effect on recombination between neomycin genes. Results are presented that are consistent with the observed stimulation of recombination occurring before plasmids integrate into the cellular DNA. Our results are discussed in relation to molecular models for extrachromosomal recombination in mammalian cells.
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Nickoloff, J. A., and R. J. Reynolds. "Transcription stimulates homologous recombination in mammalian cells." Molecular and Cellular Biology 10, no. 9 (September 1990): 4837–45. http://dx.doi.org/10.1128/mcb.10.9.4837.
Full textAbstract:
Transcription stimulates homologous recombination in Saccharomyces cerevisiae and has been implicated in the control of recombinational events during the development of mammalian immune systems. Here, we describe a plasmid-based system in which an inducible promoter from the mouse mammary tumor virus is located upstream of heteroallelic neomycin genes carried on two plasmids. Pairs of plasmids are introduced into Chinese hamster ovary cells by electroporation, and recombination is monitored by scoring colonies resistant to the aminoglycoside G418. When transcription is induced with dexamethasone, a synthetic glucocorticoid hormone, and double-strand breaks are introduced at mutation sites, recombination is stimulated sixfold over noninduced levels. Inducing transcription in circular substrates or in substrates cleaved at sites distant from the mutations has no detectable effect on recombination between neomycin genes. Results are presented that are consistent with the observed stimulation of recombination occurring before plasmids integrate into the cellular DNA. Our results are discussed in relation to molecular models for extrachromosomal recombination in mammalian cells.
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Schwarz, K., T. E. Hansen-Hagge, C. Knobloch, W. Friedrich, E. Kleihauer, and C. R. Bartram. "Severe combined immunodeficiency (SCID) in man: B cell-negative (B-) SCID patients exhibit an irregular recombination pattern at the JH locus." Journal of Experimental Medicine 174, no. 5 (November 1, 1991): 1039–48. http://dx.doi.org/10.1084/jem.174.5.1039.
Full textAbstract:
Human severe combined immunodeficiency (SCID) patients were analyzed by a polymerase chain reaction assay for their recombination capability at the DHQ52-JH region of the immunoglobulin heavy chain locus. Five patients with B cells (B+ SCID) exhibited a recombination pattern also observed in healthy persons. In contrast, six patients lacking B cells (B- SCID) showed a grossly altered rearrangement pattern characterized by the (partial) absence of regular DHQ52-JH recombinations and the presence of abnormal rearrangements. These events were caused by deletions surpassing the boundaries of immunoglobulin coding elements and thus resemble the pattern of deletional recombinations previously described in SCID mice.
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Sherratt, David J., Britta Søballe, François–Xavier Barre, Sergio Filipe, Ivy Lau, Thomas Massey, and James Yates. "Recombination and chromosome segregation." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1441 (January 29, 2004): 61–69. http://dx.doi.org/10.1098/rstb.2003.1365.
Full textAbstract:
The duplication of DNA and faithful segregation of newly replicated chromosomes at cell division is frequently dependent on recombinational processes. The rebuilding of broken or stalled replication forks is universally dependent on homologous recombination proteins. In bacteria with circular chromosomes, crossing over by homologous recombination can generate dimeric chromosomes, which cannot be segregated to daughter cells unless they are converted to monomers before cell division by the conserved Xer site–specific recombination system. Dimer resolution also requires FtsK, a division septum–located protein, which coordinates chromosome segregation with cell division, and uses the energy of ATP hydrolysis to activate the dimer resolution reaction. FtsK can also translocate DNA, facilitate synapsis of sister chromosomes and minimize entanglement and catenation of newly replicated sister chromosomes. The visualization of the replication/recombination–associated proteins, RecQ and RarA, and specific genes within living Escherichia coli cells, reveals further aspects of the processes that link replication with recombination, chromosome segregation and cell division, and provides new insight into how these may be coordinated.
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Gómez-Llanos, V., C. Morisset, J. García-Rojas, D. Jones, R. Wesson, R. L. M. Corradi, and H. M. J. Boffin. "The impact of strong recombination on temperature determination in planetary nebulae." Monthly Notices of the Royal Astronomical Society: Letters 498, no. 1 (July 21, 2020): L82—L86. http://dx.doi.org/10.1093/mnrasl/slaa131.
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ABSTRACT The long-standing difference in chemical abundances determined from optical recombination lines and collisionally excited lines raises questions about our understanding of atomic physics, as well as the assumptions made when determining physical conditions and chemical abundances in astrophysical nebulae. Here, we study the recombination contribution of [O iii] 4363 and the validity of the line ratio [O iii] 4363/4959 as a temperature diagnostic in planetary nebulae with a high abundance discrepancy. We derive a fit for the recombination coefficient of [O iii] 4363 that takes into account the radiative and dielectronic recombinations, for electron temperatures from 200 to 30 000 K. We estimate the recombination contribution of [O iii] 4363 for the planetary nebulae Abell 46 and NGC 6778 by subtracting the collisional contribution from the total observed flux. We find that the spatial distribution for the estimated recombination contribution in [O iii] 4363 follows that of the O ii 4649 recombination line, both peaking in the central regions of the nebula, especially in the case of Abell 46 that has a much higher abundance discrepancy. The estimated recombination contribution reaches up to 70 and 40 per cent of the total [O iii] 4363 observed flux, for Abell 46 and NGC 6778, respectively.
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Hiom, Kevin. "Recombination: Homologous recombination branches out." Current Biology 11, no. 7 (April 2001): R278—R280. http://dx.doi.org/10.1016/s0960-9822(01)00138-5.
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Resnick, Michael A., John Nitiss, Charles Edwards, and Robert E. Malone. "MEIOSIS CAN INDUCE RECOMBINATION IN rad52 MUTANTS OF SACCHAROMYCES CEREVISIAE." Genetics 113, no. 3 (July 1, 1986): 531–50. http://dx.doi.org/10.1093/genetics/113.3.531.
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ABSTRACT The RAD52 and RAD50 genes have previously been shown to be required for normal meiotic recombination and for various types of recombination occurring in mitotic cells. Recent evidence suggests that rad52 mutants might be defective in an intermediate recombination step; we therefore examined recombination during meiosis in several rad52 mutants at several different loci and in genetic backgrounds that yield efficient sporulation and synchronous meiosis. Similar to previous reports, spores from rad52 diploids are inviable and meiotic recombination is greatly reduced by rad52 mutations. However, intragenic recombinants were detected when cells were plated on selective media during meiosis; rad52 mutants experience induction of recombination between homologues under these special conditions. The frequencies of recombination at four loci were considerably greater than the mitotic controls; however, they were still at least 20 times lower than corresponding Rad+ strains. The prototrophs induced by meiosis in rad52 mutants were not typical meiotic recombinants because incubation in nutrient-rich medium before plating to selective medium resulted in the complete loss of recombinants. We propose that previously observed single-strand breaks that accumulate in rad52 mutants may be associated with recombinational intermediates that are resolved when cells are returned to selective mitotic media and that the meiosis-induced recombination in rad52 cells does not involve double-strand breaks.
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Shcherbakov, V. P., and L. A. Plugina. "Marker-dependent recombination in T4 bacteriophage. III. Structural prerequisites for marker discrimination." Genetics 128, no. 4 (August 1, 1991): 673–85. http://dx.doi.org/10.1093/genetics/128.4.673.
Full textAbstract:
Abstract Distance- as well as marker-dependence of genetic recombination of bacteriophage T4 was studied in crosses between rIIB mutants with known base sequences. The notion of a "basic recombination," which is the recombination within distances shorter than hybrid DNA length in the absence of mismatch repair and any marker effects, was substantiated. The basic recombination frequency per base pair can serve as an objective parameter (natural constant) of general recombination reflecting its intensity. Comparative studies of the recombination properties of rIIB mutants with various sequence changes in the mutated sites showed that the main factor determining the probability of mismatch repair in recombination heteroduplexes is the length of a continuous heterologous region. A run of A:T pairs immediately adjoining the mismatch appears to stimulate its repair. In the case of mismatches with DNA strands of unequal length, formed by frameshift mutations, the repair is asymmetric, the longer strand (bulge) being preferentially removed. A pathway for mismatch repair including sequential action of endonuclease VII (gp49)----3'----5' exonuclease (gp43)----DNA polymerase (gp43)----DNA ligase (gp30) was proposed. A possible identity of the recombinational mismatch repair mechanism to that operating to produce mutations via sequence conversion is discussed.
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Lovett, S. T., C. Luisi-DeLuca, and R. D. Kolodner. "The genetic dependence of recombination in recD mutants of Escherichia coli." Genetics 120, no. 1 (September 1, 1988): 37–45. http://dx.doi.org/10.1093/genetics/120.1.37.
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Abstract RecBCD enzyme has multiple activities including helicase, exonuclease and endonuclease activities. Mutations in the genes recB or recC, encoding two subunits of the enzyme, reduce the frequency of many types of recombinational events. Mutations in recD, encoding the third subunit, do not reduce recombination even though most of the activities of the RecBCD enzyme are severely reduced. In this study, the genetic dependence of different types of recombination in recD mutants has been investigated. The effects of mutations in genes in the RecBCD pathway (recA and recC) as well as the genes specific for the RecF pathway (recF, recJ, recN, recO, recQ, ruv and lexA) were tested on conjugational, transductional and plasmid recombination, and on UV survival. recD mutants were hyper-recombinogenic for all the monitored recombination events, especially those involving plasmids, and all recombination events in recD strains required recA and recC. In addition, unlike recD+ strains, chromosomal recombination events and the repair of UV damage to DNA in recD strains were dependent on one RecF pathway gene, recJ. Only a subset of the tested recombination events were affected by ruv, recN, recQ, recO and lexA mutations.
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Sunaga, S., K. Maki, Y. Komagata, J. Miyazaki, and K. Ikuta. "Developmentally ordered V-J recombination in mouse T cell receptor gamma locus is not perturbed by targeted deletion of the Vgamma4 gene." Journal of Immunology 158, no. 9 (May 1, 1997): 4223–28. http://dx.doi.org/10.4049/jimmunol.158.9.4223.
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Abstract Mouse TCR gamma genes in the gamma1 cluster are arranged in the order of Vgamma5, Vgamma2, Vgamma4, Vgamma3, Jgamma1, and Cgamma1 on the chromosome. During thymic ontogeny, each Vgamma gene recombines with the Jgamma1 gene in the order of proximity to Jgamma1. To explore the mechanism of the ordered recombination, we generated Vgamma4-deficient mice by gene targeting and the Cre/loxP system, by deleting the 4.8-kb DNA region between 3' of the Vgamma2 and 3' of the Vgamma4. In semiquantitative PCR analysis, Vgamma2-Jgamma1 recombination was detected frequently in adult thymus, while Vgamma3-Jgamma1 recombination preferentially occurred in fetal thymus of the mutant mice. There was no difference in the frequency of V-J recombinations between control and mutant mice. Southern blot analysis also revealed that recombination of the Vgamma2 gene occurred as frequently as in control mice. In addition, there was no difference in the levels of germline transcripts of Vgamma2 and Vgamma3 genes between control and mutant mice. Therefore, regulation of the Vgamma-Jgamma recombination was not affected by deletion of the Vgamma4 gene. These results suggest that the ordered recombination is controlled by regulatory elements near each Vgamma gene.
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Brown, Adam D., Alison B. Claybon, and Alexander J. R. Bishop. "Mouse WRN Helicase Domain Is Not Required for Spontaneous Homologous Recombination-Mediated DNA Deletion." Journal of Nucleic Acids 2010 (2010): 1–6. http://dx.doi.org/10.4061/2010/356917.
Full textAbstract:
Werner syndrome is a rare disorder that manifests as premature aging and age-related diseases.WRNis the gene mutated in WS, and is one of five human RecQ helicase family members. WS cells exhibit genomic instability and altered proliferation, andin vitrostudies suggest that WRN has a role in suppressing homologous recombination. However, more recent studies propose that other RecQ helicases (including WRN) promote early events of homologous recombination. To study the role of WRN helicase on spontaneous homologous recombination, we obtained a mouse with a deleted WRN helicase domain and combined it with thein vivopink-eyed unstable homologous recombination system. In this paper, we demonstrate that WRN helicase is not necessary for suppressing homologous recombinationin vivocontrary to previous reports using a similar mouse model.
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Poli, Riccardo, and Christopher R. Stephens. "Understanding the Biases of Generalised Recombination: Part II." Evolutionary Computation 15, no. 1 (March 2007): 95–131. http://dx.doi.org/10.1162/evco.2007.15.1.95.
Full textAbstract:
This is the second part of a two-part paper where we propose, model theoretically and study a general notion of recombination for fixed-length strings where homologous recombination, inversion, gene duplication, gene deletion, diploidy and more are just special cases. In Part I, we derived both microscopic and coarse-grained evolution equations for strings and schemata for a selecto-recombinative GA using generalised recombination, and we explained the hierarchical nature of the schema evolution equations. In this part, we provide a variety of fixed points for evolution in the case where recombination is used alone, thereby generalising Geiringer's theorem. In addition, we numerically integrate the infinite-population schema equations for some interesting problems, where selection and recombination are used together to illustrate how these operators interact. Finally, to assess by how much genetic drift can make a system deviate from the infinite-population-model predictions we discuss the results of real GA runs for the same model problems with generalised recombination, selection and finite populations of different sizes.
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Basenko, Evelina, Zeki Topcu, and Michael J. McEachern. "Recombination Can either Help Maintain Very Short Telomeres or Generate Longer Telomeres in Yeast Cells with Weak Telomerase Activity." Eukaryotic Cell 10, no. 8 (June 10, 2011): 1131–42. http://dx.doi.org/10.1128/ec.05079-11.
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ABSTRACT Yeast mutants lacking telomerase are able to elongate their telomeres through processes involving homologous recombination. In this study, we investigated telomeric recombination in several mutants that normally maintain very short telomeres due to the presence of a partially functional telomerase. The abnormal colony morphology present in some mutants was correlated with especially short average telomere length and with a requirement for RAD52 for indefinite growth. Better-growing derivatives of some of the mutants were occasionally observed and were found to have substantially elongated telomeres. These telomeres were composed of alternating patterns of mutationally tagged telomeric repeats and wild-type repeats, an outcome consistent with amplification occurring via recombination rather than telomerase. Our results suggest that recombination at telomeres can produce two distinct outcomes in the mutants we studied. In occasional cells, recombination generates substantially longer telomeres, apparently through the roll-and-spread mechanism. However, in most cells, recombination appears limited to helping to maintain very short telomeres. The latter outcome likely represents a simplified form of recombinational telomere maintenance that is independent of the generation and copying of telomeric circles.
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Choi, Koyi, Barnabas Szakal, Yu-Hung Chen, Dana Branzei, and Xiaolan Zhao. "The Smc5/6 Complex and Esc2 Influence Multiple Replication-associated Recombination Processes in Saccharomyces cerevisiae." Molecular Biology of the Cell 21, no. 13 (July 2010): 2306–14. http://dx.doi.org/10.1091/mbc.e10-01-0050.
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Replication-associated recombinational repair is important for genome duplication and cell survival under DNA damage conditions. Several nonclassical recombination factors have been implicated in this process, but their functional relationships are not clear. Here, we show that three of these factors, Mph1, Mms2, and the Shu complex, can act independently to promote the formation of recombination intermediates during impaired replication. However, their functions become detrimental when cells lack the Smc5/6 complex or Esc2. We show that mph1Δ, mms2Δ, and shu1Δ suppress the sensitivity to the replication-blocking agent methylmethane sulfonate (MMS) in smc6 mutants, with double deletions conferring stronger suppression. These deletion mutations also rescue the MMS sensitivity of esc2Δ cells. In addition, two-dimensional gel analysis demonstrates that mph1Δ, mms2Δ, and shu1Δ each reduce the level of recombination intermediates in an smc6 mutant when cells replicate in the presence of MMS, and that double deletions lead to a greater reduction. Our work thus suggests that Mph1, Mms2, and the Shu complex can function in distinct pathways in replication-associated recombinational repair and that the Smc5/6 complex and Esc2 prevent the accumulation of toxic recombination intermediates generated in these processes.
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Ebinuma, Hiroyasu. "Selective Recombination System in Bombyx mori. I. Chromosome Specificity of the Modification Effect." Genetics 117, no. 3 (November 1, 1987): 521–31. http://dx.doi.org/10.1093/genetics/117.3.521.
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ABSTRACT The effect of modifiers on recombination frequency between Ze and lem loci on chromosome 3 to elucidate the chromosome specificity of modification and the distribution of modifiers using Bombyx mori lines selected for high (H) and low (L) recombination rates between the pS and Y loci in chromosome 2 was investigated. By crossing to the Z (Ze lem/++) line, the recombination rate between the pS and Y loci in chromosome 2 was decreased from 28.18 to 23.33 in the H line and was increased from 4.92 to 16.05 in the L line. On the other hand, the recombination rate between the Ze and lem loci in chromosome 3 was increased from 16.21 to 20.21 in the Z line by crossing to the H line, but also increased to 19.02 by crossing to the L line. The significant correlation observed between the transformed recombination rates of chromosomes 2 and 3 in the (Z × L) × L backcross indicated that there were common factors modifying recombination frequency in chromosomes 2 and 3 or different factors linked to the same chromosomes. In the family of L × [(Z × L) × L] backcross, the distribution of transformed recombination rates indicated that there were several factors in the remaining chromosomes which were modifying recombination frequency in chromosome 2 but not in chromosome 3. It was also indicated that these factors were linked to different chromosomes than are the factors modifying recombination frequency in chromosome 3. In order to interpret these results, one genetic system model controlling recombination that consists of general and local recombination modifiers was proposed. The evolution of dynamic genetic systems that would effectively reduce recombinational load without reducing the advantage of recombination was discussed.
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Akamatsu, Y., N. Tsurushita, F. Nagawa, M. Matsuoka, K. Okazaki, M. Imai, and H. Sakano. "Essential residues in V(D)J recombination signals." Journal of Immunology 153, no. 10 (November 15, 1994): 4520–29. http://dx.doi.org/10.4049/jimmunol.153.10.4520.
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Abstract Recombination signal sequences for V(D)J joining consist of a conserved heptamer (CACAGTG) and a nonamer (ACAAAAACC) separated by a spacer of a constant length (12 bp or 23 bp). In the present study, we have analyzed various recombination signal mutations for their effects in V(D)J joining. Using a retroviral vector, we introduced mutant substrates stably into pre-B cells, and assayed recombination using the lacZ gene as a reporter. This method allowed us to study recombination in a single copy within the context of the host cell chromosome. Because this assay did not show any detectable background, it was quite useful in the analysis of low level recombinations. In the heptamer, mutations in the first three residues severely dropped the joining rates. Among them, the first residue adjacent to the recombination site was found to be most essential. Although mutations in the heptamer reduced the joining rate to various extents, they did not lower the site-specificity of recombination. With regard to the nonamer, the presence of three consecutive A residues was necessary for efficient recombination. Furthermore, the nucleotides flanking the A-rich core needed to be other than A residues, probably marking the border of the A-stretch. This may be important when the recombinase measures the distance between the heptamer and the nonamer to satisfy the 12/23-bp spacer rule.
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Valencia-Morales, Edgar, and David Romero. "Recombination Enhancement by Replication (RER) in Rhizobium etli." Genetics 154, no. 3 (March 1, 2000): 971–83. http://dx.doi.org/10.1093/genetics/154.3.971.
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Abstract Studies in several organisms show that recombination and replication interact closely. Recombinational repair usually requires associated replication at some stage; moreover, additional replication can induce recombination through either homologous or illegitimate events. In prokaryotes, stimulation of recombination by replication is more dramatic when rolling circle replication is employed. In contrast, θ-type replication induces only a modest increase in recombination frequency. In this article, we show that induction of θ-type replication from a supernumerary origin in the symbiotic plasmid (pSym) of Rhizobium etli leads to a 1000-fold increase in deletion formation on this plasmid. These deletions span 120 kb (the symbiotic region) and have as endpoints the reiterated nitrogenase operons. We have named this phenomenon RER, for recombination enhancement by replication. RER is not affected by the position of the replication origin in the pSym, the direction of advance of the replication fork, or the distance from the origin to the recombining repeats. On the other hand, RER is dependent on an active recA allele, indicating that it is due to homologous recombination. RER displays a strong regionality restricted to the symbiotic region. The similarities and differences of RER with the recombination process observed at the terminus of replication of the Escherichia coli chromosome are discussed.
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Friedman-Ohana, Rachel, Iris Karunker, and Amikam Cohen. "Chi-Dependent Intramolecular Recombination in Escherichia coli." Genetics 148, no. 2 (February 1, 1998): 545–57. http://dx.doi.org/10.1093/genetics/148.2.545.
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Abstract Homologous recombination in Escherichia coli is enhanced by a cis-acting octamer sequence named Chi (5′-GCTGGTGG-3′) that interacts with RecBCD. To gain insight into the mechanism of Chi-enhanced recombination, we recruited an experimental system that permits physical monitoring of intramolecular recombination by linear substrates released by in vivo restriction from infecting chimera phage. Recombination of the released substrates depended on recA, recBCD and cis-acting Chi octamers. Recombination proficiency was lowered by a xonA mutation and by mutations that inactivated the RuvABC and RecG resolution enzymes. Activity of Chi sites was influenced by their locations and by the number of Chi octamers at each site. A single Chi site stimulated recombination, but a combination of Chi sites on the two homologs was synergistic. These data suggest a role for Chi at both ends of the linear substrate. Chi was lost in all recombinational exchanges stimulated by a single Chi site. Exchanges in substrates with Chi sites on both homologs occurred in the interval between the sites as well as in the flanking interval. These observations suggest that the generation of circular products by intramolecular recombination involves Chi-dependent processing of one end by RecBCD and pairing of the processed end with its duplex homolog.
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Schierup, Mikkel H., Anders M. Mikkelsen, and Jotun Hein. "Recombination, Balancing Selection and Phylogenies in MHC and Self-Incompatibility Genes." Genetics 159, no. 4 (December 1, 2001): 1833–44. http://dx.doi.org/10.1093/genetics/159.4.1833.
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AbstractUsing a coalescent model of multiallelic balancing selection with recombination, the genealogical process as a function of recombinational distance from a site under selection is investigated. We find that the shape of the phylogenetic tree is independent of the distance to the site under selection. Only the timescale changes from the value predicted by Takahata's allelic genealogy at the site under selection, converging with increasing recombination to the timescale of the neutral coalescent. However, if nucleotide sequences are simulated over a recombining region containing a site under balancing selection, a phylogenetic tree constructed while ignoring such recombination is strongly affected. This is true even for small rates of recombination. Published studies of multiallelic balancing selection, i.e., the major histocompatibility complex (MHC) of vertebrates, gametophytic and sporophytic self-incompatibility of plants, and incompatibility of fungi, all observe allelic genealogies with unexpected shapes. We conclude that small absolute levels of recombination are compatible with these observed distortions of the shape of the allelic genealogy, suggesting a possible cause of these observations. Furthermore, we illustrate that the variance in the coalescent with recombination process makes it difficult to locate sites under selection and to estimate the selection coefficient from levels of variability.
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Nowosielska, Anetta. "Bacterial DNA repair genes and their eukaryotic homologues: 5. The role of recombination in DNA repair and genome stability." Acta Biochimica Polonica 54, no. 3 (September 23, 2007): 483–94. http://dx.doi.org/10.18388/abp.2007_3223.
Full textAbstract:
Recombinational repair is a well conserved DNA repair mechanism present in all living organisms. Repair by homologous recombination is generally accurate as it uses undamaged homologous DNA molecule as a repair template. In Escherichia coli homologous recombination repairs both the double-strand breaks and single-strand gaps in DNA. DNA double-strand breaks (DSB) can be induced upon exposure to exogenous sources such as ionizing radiation or endogenous DNA-damaging agents including reactive oxygen species (ROS) as well as during natural biological processes like conjugation. However, the bulk of double strand breaks are formed during replication fork collapse encountering an unrepaired single strand gap in DNA. Under such circumstances DNA replication on the damaged template can be resumed only if supported by homologous recombination. This functional cooperation of homologous recombination with replication machinery enables successful completion of genome duplication and faithful transmission of genetic material to a daughter cell. In eukaryotes, homologous recombination is also involved in essential biological processes such as preservation of genome integrity, DNA damage checkpoint activation, DNA damage repair, DNA replication, mating type switching, transposition, immune system development and meiosis. When unregulated, recombination can lead to genome instability and carcinogenesis.
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Saxe, Dean, Abhijit Datta, and Sue Jinks-Robertson. "Stimulation of Mitotic Recombination Events by High Levels of RNA Polymerase II Transcription in Yeast." Molecular and Cellular Biology 20, no. 15 (August 1, 2000): 5404–14. http://dx.doi.org/10.1128/mcb.20.15.5404-5414.2000.
Full textAbstract:
ABSTRACT The impact of high levels of RNA polymerase II transcription on mitotic recombination was examined using lys2 recombination substrates positioned on nonhomologous chromosomes. Substrates were used that could produce Lys+ recombinants by either a simple (noncrossover) gene conversion event or a crossover-associated recombination event, by only a simple gene conversion event, or by only a crossover event. Transcription of the lys2 substrates was regulated by the highly inducible GAL1-10 promoter or the low-level LYS2 promoter, with GAL1-10 promoter activity being controlled by the presence or absence of the Gal80p negative regulatory protein. Transcription was found to stimulate recombination in all assays used, but the level of stimulation varied depending on whether only one or both substrates were highly transcribed. In addition, there was an asymmetry in the types of recombination events observed when one substrate versus the other was highly transcribed. Finally, the lys2 substrates were positioned as direct repeats on the same chromosome and were found to exhibit a different recombinational response to high levels of transcription from that exhibited by the repeats on nonhomologous chromosomes. The relevance of these results to the mechanisms of transcription-associated recombination are discussed.