Heteroduplex deoxyribonucleic acid base mismatch repair in bacteria.

Claverys, Jean‐Pierre; Lacks, Sanford A.

doi:10.1128/mmbr.50.2.133-165.1986

Cited by 155 publications

(67 citation statements)

References 227 publications

(521 reference statements)

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“…No explanation for this difference can be offered at present. The mutSgene product plays a central role in 'proof-reading' of heteroduplex DNA, and it has been proposed to act af the mismatch recognition step (Claverys and Lacks, 1986). Unless the mutS gene product plays other hitherto unidentified roles in the cell, these results indicate that mismatch does occur in essential genes several days after growth and chromosome 10°- replication have ceased, and that these mismatches in a wild-type strain are repaired.…”

Section: Resultsmentioning

confidence: 94%

“…producing an intermediate with an old (methylated) parental strand and a new (unmethylated) mutant strand. This intermediate will eventually be recognized by the 'proof-reading' enzymes and, because of the methylation pattern, be corrected back to the parental homoduplex DNA molecule (for a review, see Claverys and Lacks, 1986). If, however, the coding strand of such heteroduplex DNA carries a mutation, it can be transcribed and translated into a mutant gene product which may allow cell growth and chromosome replication.…”

Section: Introductionmentioning

confidence: 99%

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Mechanism for induction of adaptive mutations in Escherichia coli

Boe

1990

Molecular Microbiology

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Summary When bacterial cells are subjected to a strong selective pressure it often induces specific mutations. Here a model is considered in which errors are introduced at random in one of the strands of the DNA molecule: a nick in one of the strands can initiate strand displacement rendering a region of the chromosome single‐stranded. Upon conversion back to double‐stranded DNA there is a certain probability of introducing errors creating a heteroduplex. If an error results in the production of an mRNA molecule encoding a product which provides a selective advantage, growth will be stimulated and the mutation can be immortalized by chromosomal replication. Otherwise, the error can be corrected by the DNA ‘proofreading’ enzymes.

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Section: Resultsmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Mechanism for induction of adaptive mutations in Escherichia coli

Boe

1990

Molecular Microbiology

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“…The mismatch repair system has been proven e¡ective in correcting single mismatches resulting from replication errors and recombination in both Gram-positive and Gramnegative bacteria [7,45]. It is also e¡ective in preventing recombination between mismatched sequences in S. cerevisiae [46].…”

Section: Mismatch Repair Systemmentioning

confidence: 99%

Sexual isolation in bacteria

Majewski¹

2001

FEMS Microbiology Letters

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Bacteria exchange genes rarely but are promiscuous in the choice of their genetic partners. Inter-specific recombination has the advantage of increasing genetic diversity and promoting dissemination of novel adaptations, but suffers from the negative effect of importing potentially harmful alleles from incompatible genomes. Bacterial species experience a degree of`sexual isolation' from genetically divergent organisms^recombination occurs more frequently within a species than between species. In this review, I outline the sources and mechanisms of sexual isolation within the context of selective pressures acting on different types of recombination events. ß

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“…Second, the hypothesis that genomic sequence divergence constitutes a major limitation to gene transfer between bacterial species (Matic et al, 1996) does not apply to S. pneumoniae. Whereas recombination between E. coli and Salmonella typhimurium is reduced as much as 1000-fold in mismatch repair proficient cells (Rayssiguier et al, 1989;Matic et al, 1995), in S. pneumoniae the Hex mismatch repair system, which reduces transformation frequencies for point mutations in homologous DNA (Claverys and Lacks, 1986), is unable to prevent interspecies transformation (Humbert et al, 1995). Hex is easily saturated by excess mismatches (Guild and Shoemaker, 1974;Humbert et al, 1995).…”

Section: Biological Significance Of Transformation: Genome Plasticity?mentioning

confidence: 99%

Competence‐specific induction of recA is required for full recombination proficiency during transformation in Streptococcus pneumoniae

Mortier‐Barrière

Saizieu

Claverys

et al. 1998

Molecular Microbiology

141

114

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SummaryTranscriptional activation of the recA gene of Streptococcus pneumoniae was previously shown to occur at competence. A 5.7 kb recA-specific transcript that contained at least two additional genes, cinA and dinF, was identified. We now report the complete characterization of the recA operon and investigation of the role of the competence-specific induction of recA. The 5.7 kb competence-specific recA transcript is shown to include lytA, which encodes the pneumococcal autolysin, a protein previously shown to contribute to virulence of S. pneumoniae. Uncoupling (denoted Ind ¹ ) of recA and/or the downstream genes was achieved through the placement of transcription terminators within the operon, either upstream or downstream of recA. Prevention of the competencespecific induction of recA severely affected spontaneous transformation. Transformation efficiencies of recA þ (Ind ¹ ) and of wild-type cells were compared under various conditions and with different donor DNA. Chromosomal transformation was reduced 17-(chromosomal donor) to 45-fold (recombinant plasmid donor), depending on the donor DNA, and plasmid establishment was reduced 129-fold. Measurement of uptake of radioactively labelled donor DNA in transformed cells in parallel with scoring for transformants (chromosomal donor) revealed normal uptake, but a 21-fold reduction in recombination in a recA þ (Ind ¹ ) strain, indicating that the transformation defect was primarily in recombination. Strikingly enough, a much larger (460-fold) reduction in recombination was observed for the shortest homologous donor fragment used (878 nucleotides long). Possible interpretations of the observation that basal RecA appears unable to promote efficient recombination whatever the number and the length of donor fragments taken up are proposed. The role of recA induction is discussed in view of the potential contribution of transformation to genome plasticity in this pathogen.

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Heteroduplex deoxyribonucleic acid base mismatch repair in bacteria.

Cited by 155 publications

References 227 publications

Mechanism for induction of adaptive mutations in Escherichia coli

Mechanism for induction of adaptive mutations in Escherichia coli

Sexual isolation in bacteria

Competence‐specific induction of recA is required for full recombination proficiency during transformation in Streptococcus pneumoniae

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