Unequal Crossing over

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V. V. Sukhodolets - One of the best experts on this subject based on the ideXlab platform.

  • Studying recombination in heterozygous tandem duplications in Escherichia coli
    Russian Journal of Genetics, 2007
    Co-Authors: V. V. Prokop’ev, V. V. Sukhodolets
    Abstract:

    Our previous data showed that the principal pathway of the formation of selected recombinants in Escherichia coli strains carrying heterozygous tandem duplications is Unequal Crossing over between sister chromosomes. Data presented in this work showed that when DNA homology is not disturbed (due to transposon insertion), intragenic recombinants can occur directly in the region of recombination through intrachromomal exchange as well.

  • The function of recombinations occurring in the process of DNA replication in Escherichia coli
    Russian Journal of Genetics, 2006
    Co-Authors: V. V. Sukhodolets
    Abstract:

    In a number of works dealing with the relationship between replication and recombination in bacteria, it is assumed that recombinations permit the replication forks to resume moving after having stopped at the damage sites of the template DNA. As an evidence for recombination occurring during DNA replication, the involvement in this process of proteins RuvABC and RecG, providing processing of the Holliday junctions after recombination, is considered. However, it has been shown that these proteins are not essential for resuming DNA synthesis after an exposure of bacteria to UV light. These data cast doubt on the necessity of recombination for reactivation of replication initiated in the oriC region. Studying recombination in tandem duplications in Escherichia coli showed that during replication, Unequal Crossing over occurs between direct DNA repeats of sister chromosomes. In wild strains, this Crossing over results in tandem duplications, thereby enhancing the expression of certain genes. Thus, recombination of two types occurs during DNA replication: Unequal Crossing over leading to duplications and homologous exchange, responsible for post-replication DNA repair. The Unequal exchange constitutes a component of SOS response of the cell to deterioration of the environment.

  • Unequal Crossing-over in Escherichia coli
    Genetika, 2006
    Co-Authors: V. V. Sukhodolets
    Abstract:

    Unequal Crossing-over between sister chromosomes in the process of DNA replication in Escherichia coli leads to the formation of tandem duplications, thus enhancing the activity of certain genes. In conjugational matings between genetically marked E. coli strains, Unequal Crossing-over leads to the formation of heterozygous tandem duplications. Studying these duplications as model systems allowed the conclusion that Unequal Crossing-over between direct DNA repeats of sister chromosomes is the main pathway of the formation of selected recombinants in E. coli strains carrying duplications. This was inferred from the data on the segregation of homozygous diploid recombinants by heterozygous duplications. Unequal Crossing-over between sister chromosomes occurs as adaptive exchange providing the survival of the greater part of bacterial cells on a selective medium. The known phenomenon of adaptive mutagenesis may also be a consequence of Unequal exchanges at the level of DNA mononucleotide repeats.

  • Role of recombination occurring during DNA replication
    Molecular Biology, 2006
    Co-Authors: V. V. Sukhodolets
    Abstract:

    Unequal Crossing over between direct DNA repeats of sister chromosomes occurs during DNA replication in Escherichia coli. Such exchanges yield tandem duplications and thereby increase the expression of the genes involved. Nonhomologous cohesion of sister chromosomes and Unequal Crossing over were assumed to take place when the replication fork stops. When the replication forks moves continuously, homologous exchanges between sister chromosomes ensure their postreplication repair.

  • Unequal Crossing over is the principal pathway of homologous recombination in tandem duplications of Escherichia coli
    Genetika, 2005
    Co-Authors: V. V. Prokop’ev, V. V. Sukhodolets
    Abstract:

    Homologous recombination between direct DNA repeats in tandem duplications usually leads to their dissociation. An even number of crossovers between two copies of a duplication should lead to the formation of diploid segregants, i.e., to the preservation of the duplication. However, in studies of the genotype of diploid segregants in heterozygous tandem duplications of Escherichia coli, it was shown that they arise by Unequal exchanges between sister chromosomes rather than by intrachromosomal exchanges. Generally, these exchanges lead to the establishment of the homozygous state of (heterozygous) duplications. Since the available data suggest that the exchange between sister chromosomes may be coupled with DNA replication, it is supposed that Unequal exchanges between direct DNA repeats occur in the process of DNA replication.

Akira Kakizuka - One of the best experts on this subject based on the ideXlab platform.

  • Unequal Crossing-over in Unique PABP2 Mutations in Japanese Patients: A Possible Cause of Oculopharyngeal Muscular Dystrophy
    Archives of neurology, 2002
    Co-Authors: Mika Nakamoto, Satoshi Nakano, Shingo Kawashima, Masafumi Ihara, Yo Nishimura, Akiyo Shinde, Akira Kakizuka
    Abstract:

    Background Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset autosomal dominant muscle disease with a worldwide distribution. Recent findings reveal the genetic basis of this disease to be mutations in the polyA binding–protein 2 ( PABP2 ) gene that involve short expansions of the GCG trinucleotide repeat encoding a polyalanine tract. The underlying mechanism causing the triplet-expansion mutation in PABP2 remains to be elucidated, although the DNA slippage model is thought to be a plausible explanation of that. Methods and Results We analyzed PABP2 using polymerase chain reaction analysis and DNA sequencing in Japanese patients with pathologically confirmed OPMD, and found mutated (GCG) 6 GCA(GCG) 3 (GCA) 3 GCG and (GCG) 6 (GCA) 3 (GCG) 2 (GCA) 3 GCG alleles instead of the normal (GCG) 6 (GCA) 3 GCG allele. These mutated alleles could be explained by the insertions or duplications of (GCG) 3 GCA and (GCG) 2 (GCA) 3 , respectively, but not by the simple expansion of GCG repeats. The clinical features of our patients were compatible with those of other Japanese patients carrying PABP2 that encodes a polyalanine tract of the same length, but were not compatible with those of Italian patients. Conclusions The mutated alleles identified in our Japanese patients with OPMD were most likely due to duplications of (GCG) 3 GCA and (GCG) 2 (GCA) 3 but not simple expansions of the GCG repeats. Therefore, Unequal Crossing-over of 2 PABP2 alleles, rather than DNA slippage, is probably the causative mechanism of OPMD mutations. All mutations that have been reported in patients with OPMD so far can be explained with the mechanism of Unequal Crossing-over. On the other hand, comparison of the clinical features of our patients with those of other patients in previous reports suggests that specific clinical features cannot be attributed to the length of the polyalanine tract per se.

Anna Lindstrand - One of the best experts on this subject based on the ideXlab platform.

  • Flanking complex copy number variants in the same family formed through Unequal Crossing-over during meiosis
    Mutation Research, 2018
    Co-Authors: Maria Pettersson, Jesper Eisfeldt, Elisabeth Syk Lundberg, Johanna Lundin, Anna Lindstrand
    Abstract:

    Abstract Two phenomena that have been described in germline complex genomic rearrangements (CGRs) formation are chromothripsis and chromoanasynthesis, characterized by distinct features such as the orientation and copy number of the involved fragments. Herein we present different CGRs on chromosome 5p in a mother and her daughter that through Unequal Crossing-over during meiosis has evolved from a chromothriptic rearrangement in the mother into another complex rearrangement in her daughter involving both deletions and duplications. Initially, both rearrangements were classified as simple copy number variants, but follow-up studies using whole-genome sequencing revealed a much more complex nature of both rearrangements and enabled us to decipher the biological process involved in the formation of the rearrangement found in the daughter. In conclusion, these two cases highlight the need of analyzing the inheritance patterns of CGRs, and provide an example of a disease-causing CGR formed through multiple genetic events.

Soowon Cho - One of the best experts on this subject based on the ideXlab platform.

  • Possible Role of Natural Selection in the Formation of Tandem-Repetitive Noncoding DNA
    Genetics, 1994
    Co-Authors: Wolfgang Stephan, Soowon Cho
    Abstract:

    A simulation model of sequence-dependent amplification, Unequal Crossing over and mutation is analyzed. This model predicts the spontaneous formation of tandem-repetitive patterns of noncoding DNA from arbitrary sequences for a wide range of parameter values. Natural selection is found to play an essential role in this self-organizing process. Natural selection which is modeled as a mechanism for controlling the length of a nucleotide string but not the sequence itself favors the formation of tandem-repetitive structures. Two measures of sequence heterogeneity, inter-repeat variability and repeat length, are analyzed in detail. For fixed mutation rate, both inter-repeat variability and repeat length are found to increase with decreasing rates of (Unequal) Crossing over. The results are compared with data on micro-, mini- and satellite DNAs. The properties of minisatellites and satellite DNAs resemble the simulated structures very closely. This suggests that Unequal Crossing over is a dominant long-range ordering force which keeps these arrays homogeneous even in regions of very low recombination rates, such as at satellite DNA loci. Our analysis also indicates that in regions of low rates of (Unequal) Crossing over, inter-repeat variability is maintained at a low level at the expense of much larger repeat units (multimeric repeats), which are characteristic of satellite DNA. In contrast, the microsatellite data do not fit the proposed model well, suggesting that Unequal Crossing over does not act on these very short tandem arrays.

Richard W Michelmore - One of the best experts on this subject based on the ideXlab platform.

  • recombination and spontaneous mutation at the major cluster of resistance genes in lettuce lactuca sativa
    Genetics, 2001
    Co-Authors: Doris B Chin, Rosa Arroyogarcia, Oswaldo E Ochoa, Rick Kesseli, Dean Lavelle, Richard W Michelmore
    Abstract:

    Two sets of overlapping experiments were conducted to examine recombination and spontaneous mutation events within clusters of resistance genes in lettuce. Multiple generations were screened for recombinants using PCR-based markers flanking Dm3. The Dm3 region is not highly recombinagenic, exhibiting a recombination frequency 18-fold lower than the genome average. Recombinants were identi- fied only rarely within the cluster of Dm3 homologs and no crossovers within genes were detected. Three populations were screened for spontaneous mutations in downy mildew resistance. Sixteen Dm mutants were identified corresponding to spontaneous mutation rates of 10 2 3 to 10 2 4 per generation for Dm1, Dm3, and Dm7. All mutants carried single locus, recessive mutations at the corresponding Dm locus. Eleven of the 12 Dm3 mutations were associated with large chromosome deletions. When recombination could be analyzed, deletion events were associated with exchange of flanking markers, consistent with Unequal Crossing over; however, although the number of Dm3 paralogs was changed, no novel chimeric genes were detected. One mutant was the result of a gene conversion event between Dm3 and a closely related homolog, generating a novel chimeric gene. In two families, spontaneous deletions were correlated with elevated levels of recombination. Therefore, the short-term evolution of the major cluster of resistance genes in lettuce involves several genetic mechanisms including Unequal Crossing over and gene conversion.

  • clusters of resistance genes in plants evolve by divergent selection and a birth and death process
    Genome Research, 1998
    Co-Authors: Richard W Michelmore, Blake C Meyers
    Abstract:

    : Classical genetic and molecular data show that genes determining disease resistance in plants are frequently clustered in the genome. Genes for resistance (R genes) to diverse pathogens cloned from several species encode proteins that have motifs in common. These motifs indicate that R genes are part of signal-transduction systems. Most of these R genes encode a leucine-rich repeat (LRR) region. Sequences encoding putative solvent-exposed residues in this region are hypervariable and have elevated ratios of nonsynonymous to synonymous substitutions; this suggests that they have evolved to detect variation in pathogen-derived ligands. Generation of new resistance specificities previously had been thought to involve frequent Unequal Crossing-over and gene conversions. However, comparisons between resistance haplotypes reveal that orthologs are more similar than paralogs implying a low rate of sequence homogenization from Unequal Crossing-over and gene conversion. We propose a new model adapted and expanded from one proposed for the evolution of vertebrate major histocompatibility complex and immunoglobulin gene families. Our model emphasizes divergent selection acting on arrays of solvent-exposed residues in the LRR resulting in evolution of individual R genes within a haplotype. Intergenic Unequal Crossing-over and gene conversions are important but are not the primary mechanisms generating variation.