Cloning and sequencing of Escherichia coli mutR shows its identity to topB, encoding topoisomerase III

Schofield, Mary Anne; Agbunag, Rosally; Michaels, Mark L.; Miller, Jeffrey H

doi:10.1128/jb.174.15.5168-5170.1992

Cited by 60 publications

(39 citation statements)

References 9 publications

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“…In addition, changes in DNA topology occur in starving cells (60), and supercoiling is known to influence transposition, site-specific inversions, and other types of chromosomal rearrangements (52,82,107,133). Such rearrangements may give rise to a variety of new phenotypes; for example, it is well known that cryptic genes can be activated both by insertion and by excision of IS elements (70,92,97).…”

Section: Movement Of Is Elementsmentioning

confidence: 99%

Adaptive Mutation: The Uses of Adversity

Foster¹

1993

Annual Review of Microbiology

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When populations of microorganisms are subjected to certain nonlethal selections, useful mutants arise among the nongrowing cells whereas useless mutants do not. This phenomenon, known as adaptive, directed, or selection-induced mutation, challenges the long-held belief that mutations only arise at random and without regard for utility. In recent years a growing number of studies have examined adaptive mutation in both bacteria and yeast. Although conflicts and controversies remain, the weight of the evidence indicates that adaptive mutation cannot be explained by trivial artifacts and that nondividing cells accumulate mutations in the absence of genomic replication. Because this process tends to produce only useful mutations, the cells appear to have a mech-anism for preventing useless genetic changes from occurring or for eliminating them after they occur. The model that most readily explains the evidence is that cells under stress produce genetic variants continuously and at random, but these variants are immortalized as mutations only if they allow the cell to grow.

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Section: Movement Of Is Elementsmentioning

confidence: 99%

Adaptive Mutation: The Uses of Adversity

Foster¹

1993

Annual Review of Microbiology

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“…Loss of Topo III function in E. coli similarly causes genomic instability (Schofield et al 1992) and Topo III is essential in fission yeast (Goodwin et al 1999;Maftahi et al 1999). There are two mammalian isoforms.…”

Section: Na Helicases and Topoisomerases Represent Twomentioning

confidence: 99%

The Absence of Top3 Reveals an Interaction Between the Sgs1 and Pif1 DNA Helicases inSaccharomyces cerevisiae

2006

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RecQ DNA helicases and Topo III topoisomerases have conserved genetic, physical, and functional interactions that are consistent with a model in which RecQ creates a recombination-dependent substrate that is resolved by Topo III. The phenotype associated with Topo III loss suggests that accumulation of a RecQ-created substrate is detrimental. In yeast, mutation of the TOP3 gene encoding Topo III causes pleiotropic defects that are suppressed by deletion of the RecQ homolog Sgs1. We searched for gene dosage suppressors of top3 and identified Pif1, a DNA helicase that acts with polarity opposite to that of Sgs1. Pif1 overexpression suppresses multiple top3 defects, but exacerbates sgs1 and sgs1 top3 defects. Furthermore, Pif1 helicase activity is essential in the absence of Top3 in an Sgs1-dependent manner. These data clearly demonstrate that Pif1 helicase activity is required to counteract Sgs1 helicase activity that has become uncoupled from Top3. Pif1 genetic interactions with the Sgs1-Top3 pathway are dependent upon homologous recombination. We also find that Pif1 is recruited to DNA repair foci and that the frequency of these foci is significantly increased in top3 mutants. Our results support a model in which Pif1 has a direct role in the prevention or repair of Sgs1-induced DNA damage that accumulates in top3 mutants.

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“…Recombination between 8 sequences or between rDNA sequences is also stimulated by mutations in the TOP1, TOP2, and SIR2 genes (6,15,18). In Escherichia coli, recombination between direct repeat sequences depends on RecA function (9) and is enhanced by a mutation in the topB gene (39). Albertini et al (2) proposed that in E. coli, DNA replication plays an essential role in recombination between repeated sequences by the slippedmispairing mechanism.…”

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Homologous recombination of monkey alpha-satellite repeats in an in vitro simian virus 40 replication system: possible association of recombination with DNA replication.

Kawasaki¹,

Bae²,

Eki³

et al. 1994

Mol. Cell. Biol.

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To study homologous recombination between repeated sequences in an in vitro simian virus 40 (SV40) replication system, we constructed a series of substrate DNAs that contain two identical fragments of monkey a-satellite repeats. Together with the SV40-pBR322 composite vector encoding Apr and KMr, the DNAs also contain the Escherichia coli galactokinase gene (galK) positioned between two a-satellite fragments. The a-satellite sequence used consists of multiple units of tandem 172-bp sequences which differ by microheterogeneity. The substrate DNAs were incubated in an in vitro SV40 DNA replication system and used to transform the E. coli galK strain DH1OB after digestion with DpnI. The number of E. coli galK Apr Kmr colonies which contain recombinant DNAs were determined, and their structures were analyzed. Products of equal and unequal crossovers between identical 172-bp sequences and between similar but not identical (homeologous) 172-bp sequences, respectively, were detected, although those of the equal crossover were predominant among all of the galK mutant recombinants. Similar products were also observed in the in vivo experiments with COS1 cells. The in vitro experiments showed that these recombinations were dependent on the presence of both the SV40 origin of DNA replication and SV40 large T antigen. Most of the recombinant DNAs were generated from newly synthesized DpnI-resistant DNAs. These results suggest that the homologous recombination observed in this SV40 system is associated with DNA replication and is suppressed by mismatches in heteroduplexes formed between similar but not identical sequences.It is known that the genomic DNA of higher eukaryotes, including mammals, contains large amounts of repetitive DNAs. Among them, at-satellite DNA is known to localize in centromeric regions of primate chromosomes as tandem arrays of thousands of kilobases. Homologous recombinations between these repetitive DNA sequences potentially play a crucial role in drastic chromosomal rearrangements such as chromosomal deletion, duplication, inversion, amplification, and translocation. In this context, it is surprising that such chromosomal rearrangements are usually observed very rarely in mammalian cells. The study of homologous recombination between various repetitive DNA sequences is thought to be one of the keys to understanding how chromosome integrity is maintained during the cell cycle in mammalian cells.Recent reports have shown that intrachromosomal trinucleotide repeat expansion is the cause of several human genetic diseases: myotonic dystrophy, fragile X syndrome, spinal bulbar muscular atrophy, and Huntington's disease (5, 12-14, 19, 21, 26, 31, 42). These rearrangements are thought to occur by either unequal crossing-over, i.e., crossovers between misaligned repeats, or DNA polymerase slippage, i.e., reassociation of repeats in a misaligned configuration during DNA replication. It is important to understand the mechanism of expansions or diminutions of repeats in mammalian cells.In Saccharomyces cerevis...

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Cloning and sequencing of Escherichia coli mutR shows its identity to topB, encoding topoisomerase III

Cited by 60 publications

References 9 publications

Adaptive Mutation: The Uses of Adversity

Adaptive Mutation: The Uses of Adversity

The Absence of Top3 Reveals an Interaction Between the Sgs1 and Pif1 DNA Helicases inSaccharomyces cerevisiae

Homologous recombination of monkey alpha-satellite repeats in an in vitro simian virus 40 replication system: possible association of recombination with DNA replication.

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