Biomedical subjects

Y Auffray

Publications and source records attributed to Y Auffray.

At least 55 records · Page 3Linked to original sources

PubMed1993

Partial characterization of an rpoD-like gene of Lactococcus lactis subsp. lactis ML3 with a polymerase chain reaction-based approach.

With degenerated oligonucleotide primers for conserved regions of bacterial sigma factor proteins, a 117-bp internal DNA fragment of an rpoD-like gene of Lactococcus lactis subsp. lactis ML3 was amplified by the polymerase chain reaction (PCR). The DNA sequence of this PCR product was determined by cycle sequencing, and the deduced amino acid sequence of this internal fragment showed an extensive homology with the known sigma factor sequences from six other microorganisms and present a 13-amino acid region corresponding to the typical "RpoD box" of primary sigma factors. This PCR product was used as a probe to specifically detect sigma homologs in Pediococcus acidilactici, Leuconostoc lactis, Lactobacillus helveticus, Lactobacillus acidophilus, Enterococcus faecalis, Streptococcus thermophilus, and Lactococcus lactis subsp. cremoris. These data are consistent with the existence of a high similarity between the primary sigma factors from diverse Gram-positive microorganisms.

Amino Acid Sequence↗

PubMed1992

Is thermotolerance correlated to heat-shock protein synthesis in Lactococcus lactis subsp. lactis?

Exposure of Lactococcus lactis subsp. lactis cells to a heat shock at 40 degrees C for 30 min induces thermotolerance, the increased ability of bacterial cells to survive exposure to lethal temperature (52 degrees C for 25 min). This transient state of thermal resistance is accompanied, as in Escherichia coli, by the synthesis of a new set of specific proteins termed heat-shock proteins (Hsps). Pre-treatment of the bacterial cells by antibiotics (streptomycin, spiramycin, kanamycin and erythromycin) known to act on translation, induces the major Hsps synthesis but no thermal protection; conversely, puromycin and amino acid analogues treatments, known to produce abnormal and incomplete peptides, triggers the thermotolerance state without inducing significant Hsps synthesis. These results demonstrate that heat-shock response and induced thermotolerance are not tightly correlated phenomena in L. lactis subsp. lactis.

Adaptation, Physiological↗

PubMed1991

Heat shock induces thermotolerance and inhibition of lysis in a lysogenic strain of Lactococcus lactis.

In this preliminary work, the heat shock response of lactic acid bacteria was investigated and characterized. Log-phase Lactococcus lactis cells pre-incubated at 40 degrees C before heat challenge at 52 degrees C for 30 min demonstrated increased thermotolerance as compared with cells pre-incubated at 30 degrees C. The response persisted for at least 60 min. Additionally, we demonstrated that: (i) the physiological expression of the heat shock response is temperature dependent; (ii) ethanol 4.0% (v/v) caused, to a lesser extent, a response similar to the heat shock; and (iii) hydrogen peroxide failed to induce a detectable response. Furthermore, we suggest that the induction of the heat shock response increases the resistance of a lysogenic strain of L. lactis, treated by mitomycin C (1.25 micrograms/ml), to lysis by the bacteriophage.

Ethanol↗

PubMed1989

Response of Lactococcus (Streptococcus) lactis to N-methyl-N'-nitro-N-nitrosoguanidine: absence of adaptive response.

Pretreatment of cells of Lactococcus lactis subsp. lactis with low levels of N-methyl-N'-nitro-N-nitrosoguanidine does not reduce the cytotoxic and mutagenic effects caused by high concentration of this agent. This observation indicates that there is no efficient inducible error-free repair system for alkylation damage similar to the 'adaptive response' described in detail for Escherichia coli.

Alkylating Agents↗

PubMed1988

Mutagenesis in Streptococcus lactis exposed to UV irradiation and alkylating agents.

The lethal and mutagenic effects of various mutagens on three strains of Streptococcus lactis were investigated. Lethality studies demonstrated that S. lactis was relatively sensitive to UV irradiation, methyl methanesulphonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and, to a lesser extent, to ethyl methanesulphonate (EMS). A spontaneous derivative Lac-, which has lost a 37-Md plasmid, was slightly more resistant and much less mutable than the wild-type after UV irradiation. Although the three strains were strongly mutated by EMS for the genetic marker assayed (Rifr), an increase in the mutation frequency was also observed after MMS and MNNG treatments.

Alkylating Agents↗

PubMed1987

Genotoxic activity of some mycotoxins using the SOS chromotest.

The genotoxic activity of 11 mycotoxins was investigated in Escherichia coli K 12. The induction of the SOS function sfi A whose level of expression is monitored by means of a sfi A::lac Z operon fusion was assayed by measuring the beta-galactosidase activity in the PQ 37 strain. Most of these fungal metabolites did not induce SOS response in this bacterial test. Only aflatoxicol, a reduced metabolite of aflatoxin B1 was well detected as an SOS inducer if metabolic activation was performed. Patulin, penicillic acid and viomellein are only weak inducing agents. The other fungal compounds tested failed to demonstrate a positive SOS inducing activity. Relationship between SOS chromotest, mutagenicity to Salmonella typhimurium and in vivo carcinogenicity was discussed.

Colorimetry↗

PubMed1987

Evidence that N-methyl-N'-nitro-N-nitrosoguanidine induces adaptive response in Bacillus thuringiensis.

Bacillus thuringiensis is shown to have an inducible error-free repair system for alkylation damage as found in Escherichia coli and Bacillus subtilis. Growth of cells in the presence of low concentrations of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces an adaptive response which is characterized by an increase in resistance to killing and mutagenesis by challenge with higher concentrations of MNNG. In addition, we have noted with interest that adaptive low doses seem to produce lesions at a rate sufficient to induce an increase of mutation frequency, and inhibition of cell division. The possibility of an interaction between SOS and adaptive responses with these low doses of MNNG is discussed.

Adaptation, Physiological↗

PubMed1987

Presence of inducible DNA repair in Bacillus thuringiensis.

Weigle reactivation of ultraviolet-irradiated luminal diameter 8 bacteriophage was observed after ultraviolet treatment of Bacillus thuringiensis cells. A slight increased frequency of clear plaque mutants was detected among the survivors. The kinetics of induction of the phage reactivation and phage mutagenesis have been determined. The presence of chloramphenicol before and after irradiation abolished the induction of repair and mutagenesis. These experiments suggest that, in spite of the relatively small mutagenic response in bacteriophage progeny, B. thuringiensis has an inducible repair system responsible to the significant Weigle reactivation of irradiated phage.

Bacillus thuringiensis↗

PubMed1987

U.v.-induced and N-methyl-N'-nitro-N-nitrosoguanidine-induced mutagenesis in Bacillus thuringiensis.

The lethal and mutagenic effects of u.v. light and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on Bacillus thuringiensis were investigated. Lethality studies demonstrated that B. thuringiensis was relatively sensitive to these agents. This bacterium was mutated at the rifampicin resistance marker by u.v. light and to a lesser extent by the direct acting alkylating agent MNNG. One mutant selected for its greater sensitivity to u.v. light expressed a higher frequency of mutagenesis after u.v. light treatment and appeared to be defective in an excision repair pathway. However, this mutant was only slightly mutable by MNNG in comparison with the wild-type strain. This unusual phenotype does not yet have a parallel among the radiation sensitive mutants described in other bacterial species.

Bacillus thuringiensis↗

PubMed1987

[Directional osteotomy of the femur in the bedridden patient with cerebral palsy].

Wind-blown or scissor deformity of the hip in severely spastic bed-ridden patients with cerebral palsy requires surgical correction. The methods generally used involve a number of disadvantages which are analysed. Corrective sub-trochanteric osteotomy following extensive soft tissue release is the method of choice in this exceptional situation. The treatment of six patients since 1982 has emphasised the good tolerance of this operation by patients who are frail and suffer from multiple handicaps and the reliability of the results obtained in the relief of pain, the improved ease of nursing management and attention to toilet and, in certain cases, the ability to sit.

Adolescent↗

PubMed1985

Prophage induction and filamentation in Bacillus thuringiensis caused by the genotoxic mycotoxin aflatoxin B1.

Cultures of the lysogenic strain of Bacillus thuringiensis var. tolworthi were made in the presence of various drugs. The determination of bacterial size and plaque forming units (by using an indicator strain of B. thuringiensis var. galleriae) as well as colony forming units were then performed. Treatment of lysogenic cells by aflatoxin B1: provokes the formation of elongated cells (filamentation); induces a pathway that leads to the induction of prophage. Results of the present study indicated that filament formation and bacteriophage induction are two commonplace effects that occur in virtually every member of this cellular population exposed to low doses of certain drugs such as aflatoxin B1 (10 micrograms/ml); all of which have in common the ability to produce damaging changes in DNA. The following findings support the hypothesis that error-prone repair mechanisms seem to be present in B. thuringiensis as in Escherichia coli.

Aflatoxin B1↗

PubMed1984

[Antibacterial and genotoxic properties of 33 mycotoxins].

Most of the 33 fungal metabolites tested provoke: Bacterial growth inhibition of Bacillus thuringiensis similar to lethal effect of antibiotics. Positive response in the 'Rec' assay using strains of Bacillus subtilis; this fact shows that these toxins are DNA modifying agents. Enlargement of cell volume in the first bacteria species; this cell-abnormality induction resembles those obtained with mitomycin C. Correlation between elongation of cells (filamentation) and in vivo carcinogenicity of mycotoxins is discussed. The filamentation should be an expression of a perturbated DNA replication (S.O.S.-error prone repair) as the consequence of DNA damages induced by genotoxic agents (i.e. carcinogens).

Bacillus subtilis↗

PubMed1977

[Antibacterial properties of aflatoxin B1: cytotoxic effects on Bacilus thuringiensis (Berliner)].

In a sensitive strain of Bacillus thuringiensis (Berliner), aflatoxin B1 inhibited growth with a dose above 5.0 microgram/ml. With subinhibitory levels (0.5 - 5.0 microgram/ml) physiological damage (decreased growth rate) and cellular alteration (filamentous cells) were noted. With these doses the mycotoxin disturbs various metabolisms : DNA synthesis (gradual blockage of the specific bacteriophage multiplication and dispersion of nuclear apparatus in giant cells); protein synthesis (decrease of protease secretion (2.0 microgram/ml), thuricin excretion (3.0 microgram/ml) and inhibition of endotoxin formation (4.0 microgram/ml); specific activities (bacterial motility, flagellar arrangment and sporulation were respectively affected with 1.0, 0.5 and 4.0 microgram/ml). The mycotoxin did not affect the metabolism of a resistant mutant isolated in the presence of a lethal dose of aflatoxin B1 (mutation rate : 1.10(8) with 20 microgram/ml). The numerous bacterial responses to aflatoxin B1 indicate that the probable site of its toxic binding may not be restricted to a particular locus on the DNA. On the contrary these observations suggest that there exist many combining affinities of the mycotoxin for intracellular sites or interference with a key-function such as the messenger-RNA synthesis.

Aflatoxins↗

PubMed1975

[Inhibition of cytotoxic effects of B1 aflatoxin towards the bacterial cell by coumarin. Role of other interfering factors].

The coumarin has with some limits a repressive effect on the antibacterial power of Aflatowin B1. It behaves towards cells of Bacillus thuringiensis (Berliner) treated by the myocotoxic, like a curative agent. Therefore, the reaction of microbial cells on the cytotoxic effect of Aflatoxin B1 depends on the aeration of the culture and chiefly on the "inoculum effect".

Aflatoxins↗

PubMed1972