Mismatch repair in Streptococcus pneumoniae: relationship between base mismatches and transformation efficiencies.

Claverys, Jean‐Pierre; Méjean, Vincent; Gasc, Anne-Marie; Sicard, A M

doi:10.1073/pnas.80.19.5956

Cited by 75 publications

(60 citation statements)

References 28 publications

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“…In strain MW3317-21A, however, the line between high and intermediate efficiency is ill defined, and no subdivision can be made for strain MW3271-1OC-arg4A, This may be an effect of different genetic backgrounds (see Discussion). The order of repair efficiencies, including the possible subdivision of the second class, correlates with the order determined for E. coli in vivo (17,34) and in vitro (57) as well as for S. pneumoniae (13,36) (see also Discussion).…”

Section: Resultsmentioning

confidence: 99%

Heteroduplex DNA correction in Saccharomyces cerevisiae is mismatch specific and requires functional PMS genes.

Kramer¹,

Kramer²,

Williamson³

et al. 1989

Mol. Cell. Biol.

160

117

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a high to intermediate efficiency. The mismatch C/C and a 38-nucleotide loop were corrected with low efficiency. This substrate specificity pattern resembles that found in Escherichia coli and Streptococcus pneumoniae, suggesting an evolutionary relationship of DNA mismatch repair in pro-and eucaryotes. Repair of the listed mismatches was severely impaired in the putative S. cerevisiae DNA mismatch repair mutants pmsl and pms2. Low-efficiency repair also characterized pms3 strains, except that correction of single-nucleotide loops occurred with an efficiency close to that of PMS wild-type strains. A close correlation was found between the repair efficiencies determined in this study and the observed postmeiotic segregation frequencies of alleles with known DNA sequence. This suggests an involvement of DNA mismatch repair in recombination and gene conversion in S. cerevisiae.

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Section: Resultsmentioning

confidence: 99%

Heteroduplex DNA correction in Saccharomyces cerevisiae is mismatch specific and requires functional PMS genes.

Kramer¹,

Kramer²,

Williamson³

et al. 1989

Mol. Cell. Biol.

160

117

View full text Add to dashboard Cite

show abstract

“…Because C⅐C mismatches are not recognized by MMR in other bacterial species (20,44), this particular feature of oligo recombination might have the potential to create high recombination frequencies in other bacteria. For this reason and others, the ability to transfer the homologous recombination system to other bacterial species and even to eukaryotes would be very useful.…”

Section: Discussionmentioning

confidence: 99%

Enhanced levels of λ Red-mediated recombinants in mismatch repair mutants

Costantino

Court

2003

Proc. Natl. Acad. Sci. U.S.A.

265

359

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Homologous recombination can be used to generate recombinants on episomes or directly on the Escherichia coli chromosome with PCR products or synthetic single-stranded DNA (ssDNA) oligonucleotides (oligos). Such recombination is possible because bacteriophage -encoded functions, called Red, efficiently recombine linear DNA with homologies as short as 20 -70 bases. This technology, termed recombineering, provides ways to modify genes and segments of the chromosome as well as to study homologous recombination mechanisms. The Red Beta function, which binds and anneals ssDNA to complementary ssDNA, is able to recombine 70-base oligos with the chromosome. In E. coli, methyl-directed mismatch repair (MMR) can affect these ssDNA recombination events by eliminating the recombinant allele and restoring the original sequence. In so doing, MMR can reduce the apparent recombination frequency by >100-fold. In the absence of MMR, Red-mediated oligo recombination can incorporate a single base change into the chromosome in an unprecedented 25% of cells surviving electroporation. Our results show that Beta is the only bacteriophage function required for this level of recombination and suggest that Beta directs the ssDNA to the replication fork as it passes the target sequence. H omologous recombination mediated by Red has been used as a genetic tool to modify the bacterial chromosome with linear double-stranded DNA (dsDNA) (1-6). In addition to linear dsDNA, single-stranded DNA (ssDNA) oligonucleotides (oligos) have been used to modify the chromosomes of both yeast and Escherichia coli (7-9). In yeast, the functions are not yet defined that allow oligo recombination; however, in E. coli, the bacteriophage Red recombination system is involved (9).The Red system includes the Gam, Exo, and Beta proteins. Whereas Red-mediated recombination between linear duplex DNA and the bacterial chromosome requires all three functions (1, 3, 10), recombination with ssDNA oligos requires only the Beta protein (9). Beta protein binds stably to ssDNA (11) Ͼ35 nt in length (12), protects it from single-strand nuclease attack (13,14), and promotes annealing to complementary ssDNA (13-15).Beta binds ssDNA from 3Ј to 5Ј (13, 16) but does not bind directly to dsDNA (13,14). However, after Beta generates dsDNA by annealing two complementary ssDNAs, it remains tightly bound to the annealed dsDNA (13,14,16). As it anneals strands to form the dsDNA, it generates DNA filaments similar to those formed by . This annealed dsDNA-Beta complex is resistant to DNase I and is much more stable than the ssDNA-Beta complex (16).Although Beta can catalyze single-strand annealing, it cannot promote strand invasion of a duplex DNA with a homologous ssDNA during recombination (16,18). Therefore, Betamediated recombination with ssDNA is likely to occur by annealing with transiently single-stranded regions of the chromosome. Initial results suggest that Beta-dependent ssDNA recombination may occur at the DNA replication fork. When either of the two complementary ssDNA oligos...

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“…G-T and G··A mismatches are among the more stable mispairs, while A-C and C-C fall into the least stable class. By contrast, G-T and A-C transition mispairs are usually well repaired, while G-A and C-C transversion mis matches are generally poor substrates (28,29,(59)(60)(61) . In fact, the sequences of the 16 octadecamer duplexes studied by Wemtges et al (77) corresponded to a set of M13 heteroduplexes used in a previous study to assess efficiencies of correction in vivo (28) .…”

Section: Structures Of Base Pair Mismatchesmentioning

confidence: 99%

“…The G-T and A-C transition mismatches are good substrates fo r repair in both organisms (27, 28, 59-6 1). A-A, G-G , and T-T transversion mispairs are also subject to correction in both organisms (60,61), as are the four possible mismatches corresponding to insertiOn/deletion of A, G, C, or T (59, 62), although this group of mismatches is recognized somewhat less well than the transition mispairs (28,59,60). Insertions/deletions of 10 nuc1eotides are also corrected in E. coli (58), but in those cases tested , mismatches involving larger regions of noncomplementarity (> 30 base pairs in S. pneumoniae, 800 base pairs in E. coli) were found to be refractory to repair (29,59,60).…”

Section: Mismatch Specificitymentioning

confidence: 99%