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Biomedical subjects

A M Gasc

Publications and source records attributed to A M Gasc.

25 records · Page 2Linked to original sources
PubMed1981

Base specificity of mismatch repair in Streptococcus pneumoniae.

DNA sequence analysis was undertaken to investigate the structural basis of mutations showing different integration efficiencies in Streptococcus pneumoniae. Wild type, mutant and revertant sequences at two sites in the amiA locus were determined. It appears that markers which transform efficiently or inefficiently can result from single base pair changes. A low efficiency (LE) marker corresponds to a C:G to T:A change and a high efficiency (HE) marker to a G:C to T:A change. In the latter case, two mismatches, G/A and T/C, can exist at the heteroduplex stage in transformation; only T/C appears to be recognized by the hex system which controls transforming efficiencies in pneumococcus. Each of the recognized mismatches, T/G and C/A, which result from transitional change, and T/C appears to involve at least one pyrimidine. It is proposed that the mismatch repair system of S. pneumoniae is directed against mismatched pyrimidines. DNA sequence analysis also reveals that short deletions (33 or 34 bases long) behave as very high efficiency markers, confirming that deletions are not recognized by the hex system.

Base Composition↗
PubMed1980

Lack of SOS repair in Streptococcus pneumoniae.

Wild-type strains of Streptococcus pneumoniae were non-mutable by UV radiation and thymidine starvation. Moreover, UV-irradiated pneumococcal omega 2 phages were not reactivated in an irradiated host. This suggests that, in pneumoococcus, there is no efficient inducible repair process similar to the SOS repair described in detail for E. coli. We also report that mutations cannot be induced by a process thought to be linked to competence during transformation with isogenic wild-type DNA either on wild-type strains or in strains in which the hex function of excision and repair of mismatched bases is inactive.

Bacteriophages↗
PubMed1979

Characterization of an amber suppressor in Pneumococcus.

Partial revertant has been isolated, with resistance to aminopterin intermediate between wild type and mutant. This phenotype is the result of a mutation at a gene unlinked to the amiA locus. This suppressor mutation (su+) has no phenotypic characteristics by itself except a slow growth. 9 amiA mutants (belonging to 6 sites) are affected by su+ out of the 30 investigated mutants (i.e. 22 sites). The efficiency of suppression is site dependent. Two sites out of 14 mutants belonging to the thymidylate synthetase gene are suppressible. Thymidylate synthetase activity is partially restored by su+. Optochin mutants can also be suppressed. Thus su+ is not gene specific but site specific. Moreover when the str-41 allele conferring resistance to streptomycin is introduced by transformation, the suppression effect is restricted. All these properties are characteristic of an informational suppressor. The t-RNA extracted from the suppressor strain su+ but not the wild type restored the synthesis of coat protein coded by RNA from an amber mutant of bacteriophage f2. Attempts to detect ochre suppression activity gave negative results. It is suggested that the su+ gene is amber specific. Thus su+ can provide insight into the nature of suppressible mutations which should be point mutations. Both low efficiency and high efficiency mutants are affected by su+; this is additional evidence that both categories contain point mutations.

Alleles↗
PubMed1978

Genetic studies of acridine-induced mutants in Streptococcus pneumoniae.

The mutagenic properties of acridines on pneumococcus are described. All seven acridines tested were mutagenic at the amiA locus conferring a resistance to 10(-5) M aminopterin. The effects of quinacrine were more specifically investigated. It was observed that: mutants can be obtained only by treatment of exponentially growing cells; a sharp maximum mutagenic effect occurs at a concentration slightly lower than the bacteriostatic value; and the amount of quinacrine required to yield the maximum mutagenic effect decreases with the pH of the medium. Moreover, the number of mutants detected after quinacrine treatment varies from locus to locus. The majority of quinacrine-induced mutants are readily reverted by quinacrine, but not by nitrosoguanidine treatment. This suggests that in pneumococcus quinacrine induces mainly frameshift mutations. A further study of the revertants obtained by quinacrine treatment of quinacrine-induced mutants strengths this interpretation: most of the revertants result from a mutation at the same site; some partial revertants exhibiting an intermediate resistance to aminopterin were found to contain two very closely linked mutated sites, each mutation conferring the maximum level of resistance to aminopterin. Thus, the majority of quinacrine-induced mutants at the amiA locus of pneumococcus consists of frameshift mutations. Nearly all of the isolated mutants induced by quinacrine as well as other acridines belong to the low efficiency class of transformation. It was concluded that the mismatch resulting from the pairing between the wild type and the frameshift-containing sequence is recognized by the excision-repair system involved in the discrimination function in a way similar to that in which it recognizes mismatched base pairs between a transition mutation and the wild-type sequence.

Acridines↗
PubMedDate not supplied

Long- and short-patch gene conversions in Streptococcus pneumoniae transformation.

In pneumococcal transformation some point mutations are integrated by an excision-repair pathway which switches the heteroduplex DNA into homoduplex. This transfer of information is a gene conversion. We have reviewed some of the properties of this system especially those relating to heteroduplex specificity and given evidence that this extends over several kilobases of DNA. We then describe a new process of conversion in pneumococcal transformation which occurs over a very short distance (5 to 27 base-pairs) and is triggered by a single site mutation resulting from the transversion 5'-ATTCAT...to 5'...ATTAAT... Only one of the two heteroduplexes 5'...A...3'/3'...G...5', is converted.

Base Sequence↗
PubMedDate not supplied

Molecular biology of Streptococcus pneumoniae: an everlasting challenge.

Streptococcus pneumoniae is a model for elucidating: 1) recombination steps of DNA, from its discovery to polarity of integration; 2) long-patch mismatch repair, short-patch repair triggered by A/G and exclusion of deletions; 3) resistance to beta-lactam antibiotics; and 4) factors of virulence. Several of these topics remain a challenge for future investigations.

Animals↗