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M Defais

Publications and source records attributed to M Defais.

47 records · Page 3Linked to original sources
PubMed1977

Kinetics of induction of error-prone repair of bacteriophage lambda by temperature shift in an Escherichia coli dnaB mutant.

Preincubation at 42 degrees, before infection at permissive temperature by phage lambda, of an Escherichia coli dnaB mutant, provokes a significant increase in survival and mutagenesis of ultraviolet irradiated phage as well as mutagenesis of untreated phage. Similarly to UV irradiation and many chemical mutagens, the inhibition of DNA synthesis by temperature shift of this dnaB mutant induces SOS repair. This work shows that replication blockage in bacterial DNA is not only mutagenic for bacterial DNA itself (Witkin, 1975) but also for normally replicating lambda DNA, probably due to induction of diffusible products.

Coliphages↗
PubMed1977

Phage yield during W-reactivation of bacteriophage.

Phage production in liquid medium during W-reactivation parallels the extent of W-reactivation of infective centres on plates. The mean burst size is independent of W-reactivation; thus the reactivated phage yields a normal burst. As 8 plates, the lex- mutant shows no W-reactivation in liquid medium. It is concluded that W-reactivation is a consequence of an induced DNA repair which reactivates the damaged parental phage DNA to its full biological activity.

Cell Count↗
PubMed1976

Induction kinetics of mutagenic DNA repair activity in E. coli following ultraviolet irradiation.

Ultraviolet mutagenesis of phage gamma is produced by host functions which are inducible by ultraviolet irradiation of the host cell. Induction kinetics and the half life of the inducible mutagenic DNA repair (SOS-repair) in E.coli have been determined using phage gamma assays. At 37 degrees C, both mutagenic and repair activities are maximal approximately 30 min following irradiation and decay with a half life of approximately 30 min. The presence of 100 mug/ml chloramphenicol during the first 40 min after irradiation completely abolishes induction of repair and mutagenesis. The ultraviolet induction pattern of SOS repair very much resembles that of gamma prophage in lysogenic induction (Monk and Kinross, 1975).

Chloramphenicol↗
PubMedDate not supplied

Enhanced mutagenesis during post-treatment incubation of Escherichia coli treated with cis-diamminedichloroplatinum(II).

Wild-type Escherichia coli were treated with cis-dichlorodiammineplatinum(II) (DDP) and then kept in a non-dividing state for 4 h. This post-treatment incubation did not increase survival, excision of platinum-DNA lesions was not observed, and post-treatment exposure to thiourea had no effect on the toxicity of DDP. In contrast, the mutation frequency increased by a factor of 3 and reached a plateau after 3 h incubation at 37 degrees C. The quantity of DDP on the bacterial DNA remained constant during this time. Post-treatment exposure to thiourea (which is reported to react with monofunctional platinum-DNA adducts) inhibited but did not reverse the increased mutagenicity. These results may reflect the evolution of monofunctional platinum-DNA lesions into bifunctional mutagenic adducts during post-treatment incubation of bacteria which have been exposed to DDP.

Cell Division↗
PubMedDate not supplied

Repair of platinum-DNA lesions in E. coli by a pathway which does not recognize DNA damage caused by MNNG or UV light.

The adaptive response is an inducible DNA-repair system which diminishes the mutagenic and toxic effects of alkylating agents. A mutant of E. coli constitutive for adaptative repair, BS21, has been isolated. A spontaneous revertant of this strain, BS23, lacks the adaptive response. When compared to its wild-type parent, mutant BS21 showed an increased resistance to the killing and mutagenic effects of a compound which is not a classical alkylating agent, the antitumor drug cis-diamminedichloroplatinum(II) (cis-DDP). However, this resistance to cis-DDP was also found in strain BS23 which lacks the adaptive response. cis-DDP bound to the DNA of all 3 strains with the same efficiency. In addition, we have investigated the effect of UV radiation and we failed to observe a significant difference in the survival and mutagenesis of these strains. This evidence suggests that the resistance of BS21 and BS23 strains to cis-DDP is not a consequence of the adaptive response or increased excision repair.

Cisplatin↗
PubMedDate not supplied

Site-directed mutagenesis in the Escherichia coli recA gene.

Escherichia coli RecA protein plays a fundamental role in genetic recombination and in regulation and expression of the SOS response. We have constructed 6 mutants in the recA gene by site-directed mutagenesis, 5 of which were located in the vicinity of the recA430 mutation responsible for a coprotease deficient phenotype and one which was at the Tyr 264 site. We have analysed the capacity of these mutants to accomplish recombination and to express SOS functions. Our results suggest that the region including amino acid 204 and at least 7 amino acids downstream interacts not only with LexA protein but also with ATP. In addition, the mutation at Tyr 264 shows that this amino acid is essential for RecA activities in vivo, probably because of its involvement in an ATP binding site, as previously shown in vitro.

Bacterial Proteins↗
PubMedDate not supplied

RECA immunological assay as a tool to analyze the SOS response.

The content of RECA protein, one of the SOS genes product, was determined in a bacterial extract by a two site-radioimmunometric assay. The variation of the RECA concentration after induction by physical or chemical treatments was used as a probe to analyze the SOS response. Relationships between either the number or the nature of DNA lesions and the level of the relative amplification of RECA have been established. The modulation of the recA gene expression is discussed.

DNA Repair↗
PubMedDate not supplied

The adaptive response in E. coli.

The adaptive response appears in E. coli after exposure to low levels of alkylating agents. This system is under the positive control of the ada gene. At least two enzymes are induced during the response: 3-methyladenine DNA glycosylase II and O6-methylguanine DNA methyltransferase. The latter is also the product of the ada gene.

Adenine↗