Molecular Evolution of Rifampicin Resistance in<i>Streptococcus pneumoniae</i>

Enright, Mark C.; Zawadski, Piotr; Pickerill, Paul; Dowson, Christopher G.

doi:10.1089/mdr.1998.4.65

Cited by 44 publications

(41 citation statements)

References 28 publications

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“…The determination of the DNA changes which arise in independent Rif r mutants should reveal the mutator specificity of the strain 800T51. Searching the pneumococcal genome sequence (with the TIGR database) indicates that cluster I is almost identical in pneumococcus and other bacteria, as confirmed recently by Enright et al (9). A 1,500-bp segment including cluster I was amplified in independent Rif r mutants.…”

Section: Resultssupporting

confidence: 54%

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Hyperrecombination in Streptococcus pneumoniae Depends on an Atypical mutY Homologue

Samrakandi

Pasta

2000

J Bacteriol

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The unusual behavior of the mutation ami36, which generates hyperrecombination in two point crosses, was previously attributed to a localized conversion process changing A/G mispairs into CG pairs. Although the mechanism was found to be dependent on the DNA polymerase I, the specific function responsible for this correction was still unknown. Analysis of the pneumococcal genome sequence has revealed the presence of an open reading frame homologous to the gene mutY of Escherichia coli. The gene mutY encodes an adenine glycosylase active on A/G and A/7,8-dihydro-8-oxoguanine (8-OxoG) mismatches, inducing their repair to CG and C/8-OxoG, respectively. Here we report that disrupting the pneumococcal mutY homologue abolishes the hyperrecombination induced by ami36 and leads to a mutator phenotype specifically enhancing AT-to-CG transversions. The deduced amino acid sequence of the pneumococcal MutY protein reveals the absence of four cysteines, highly conserved in the endonuclease III/MutY glycosylase family, which ligate a [4Fe-4S] 2؉ cluster. The actual function of this cluster is still intriguing, inasmuch as we show that the pneumococcal gene complements a mutY strain of E. coli.In transformation of Streptococcus pneumoniae, doublestranded DNA binds to the membrane and is randomly cleaved (see reference 23 for a review). Then, single-stranded segments enter the cell from a 3Ј end while the complementary strands are degraded to oligonucleotides with the opposite polarity (32). About half of the entering segments integrate into the chromosome by homologous recombination (21). The recombination process is RecA dependent (37), exchanges strands from 5Ј to 3Ј relative to the donor (43), and forms a donorrecipient structure which is heteroduplex when the donor and the recipient sequences are not identical (11). Both strands of the donor DNA have the same probability of entering a cell so that two complementary heteroduplexes are generated in equal frequency among the recipient bacteria (7). Pneumococcal transformation therefore allows study of the in vivo processing of heteroduplexes such as base-base mismatches. In particular, the variability observed in the transformation efficiencies of point mutations led to the discovery of a mismatch repair system (10,20,55). This system, called Hex, recognizes the different mismatches with varying efficiencies and induces the complete excision of the donor strand (31). Base mismatches are ranked as a function of decreasing repair efficiency by Hex as follows: (6). The deletions and the additions of one or two nucleotides lead to mismatches that are very efficiently recognized by Hex (13,14). The heterologies longer than 2 bases lead to heteroduplexes which are poorly recognized by Hex, and for those longer than 5 bases, there is no repair at all by Hex (13,22) nor by any bacterial repair or conversion system (42).A Hex-independent repair, specific for A/G mismatches, was found in S. pneumoniae. The existence of such a system was signalled by the hyperrecombination-i.e., the abn...

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Section: Resultssupporting

confidence: 54%

“…Out of 23 independent Rif r mutants, the mutations were found on three codons of cluster I, among which was the codon for serine 495 (Table 5). Rif r mutations in this codon were previously reported in E. coli but not in S. pneumoniae (9,19). We have detected GC-to-TA (and CG-to-AT) transversions in three types of Rif r mutants out of five types characterized.…”

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confidence: 54%

Hyperrecombination in Streptococcus pneumoniae Depends on an Atypical mutY Homologue

Samrakandi

Pasta

2000

J Bacteriol

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“…Among the rifampin-resistant donors, we noted His526 substitutions, also known to confer resistance in Bacillus, Mycobacterium, and Escherichia (8,30). We identified Asp526 (S. pneumoniae Pn16, S. intermedius) and Tyr526 (Streptococcus oralis, S. pneumoniae strain R6, S. pneumoniae strain 96129) substitutions.…”

Section: Methodsmentioning

confidence: 93%

Barriers to Genetic Exchange between Bacterial Species: Streptococcus pneumoniae Transformation

et al. 2000

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Interspecies genetic exchange is an important evolutionary mechanism in bacteria. It allows rapid acquisition of novel functions by transmission of adaptive genes between related species. However, the frequency of homologous recombination between bacterial species decreases sharply with the extent of DNA sequence divergence between the donor and the recipient. In Bacillus and Escherichia, this sexual isolation has been shown to be an exponential function of sequence divergence. Here we demonstrate that sexual isolation in transformation between Streptococcus pneumoniae recipient strains and donor DNA from related strains and species follows the described exponential relationship. We show that the Hex mismatch repair system poses a significant barrier to recombination over the entire range of sequence divergence (0.6 to 27%) investigated. Although mismatch repair becomes partially saturated, it is responsible for 34% of the observed sexual isolation. This is greater than the role of mismatch repair in Bacillus but less than that in Escherichia. The remaining non-Hex-mediated barrier to recombination can be provided by a variety of mechanisms. We discuss the possible additional mechanisms of sexual isolation, in view of earlier findings from Bacillus, Escherichia, and Streptococcus.Bacteria from all major taxa are able to exchange genes across species by homologous recombination (26). While the various bacteria take up donor DNA by a diversity of mechanisms, all studied systems of homologous recombination share at least one homologous feature: recombination depends ultimately on the activity of the RecA protein and its homologues (26). Similarly, there is one system that hinders recombination across species in both the Proteobacteria and the gram-positive bacteria (3). This is the mismatch repair system encoded by mutS, mutL, and their homologues. Because some of the molecular basis for interspecies recombination is shared across disparate taxa, we might expect that recombination between species is constrained in similar ways throughout the bacterial world.In addition, previous studies have shown that the frequency of homologous recombination decreases with the sequence divergence between donor and recipient, in a manner that is similar across a wide range of organisms. In Bacillus transformation as well as in Escherichia conjugation, the frequency of recombination decreases exponentially with the degree of DNA sequence divergence between donor and recipient (23,28,31). A similar exponential relationship has been observed for the frequency of intrachromosomal crossovers in Saccharomyces cerevisiae (5). Nevertheless, the major mechanisms producing recombinational barriers have been shown to differ in each of the above cases. In Escherichia coli, the predominant barrier to recombination is presented by the methylation-directed mismatch repair system (21). In Bacillus, mismatch repair is only marginally effective in preventing recombination between divergent sequences; the most significant barrier is that donor stran...

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“…It has been reported that rifampicin resistance could be acquired due to an RNA polymerase single point mutation. 34,35) These two strains may be candidates for selected rifampicin-resistant mutants. The isolates of B. animalis subsp.…”

Section: Discussionmentioning

confidence: 99%

Antibiotic Susceptibility of Bifidobacterial Strains Distributed in the Japanese Market

Xiao

Takahashi

Odamaki

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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Molecular Evolution of Rifampicin Resistance inStreptococcus pneumoniae

Cited by 44 publications

References 28 publications

Hyperrecombination in Streptococcus pneumoniae Depends on an Atypical mutY Homologue

Hyperrecombination in Streptococcus pneumoniae Depends on an Atypical mutY Homologue

Barriers to Genetic Exchange between Bacterial Species: Streptococcus pneumoniae Transformation

Antibiotic Susceptibility of Bifidobacterial Strains Distributed in the Japanese Market

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