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L V Konevega

Publications and source records attributed to L V Konevega.

14 recordsLinked to original sources
PubMed2000

Mutagenic effects of gamma-rays and incorporated 8-3H-purines on extracellular lambda phage: influence of mutY and mutM host mutations.

The lethal and mutagenic effects on phage lambdacI857 of 60Co gamma-rays and of decay of 3H incorporated into phage DNA both as 8-3H-deoxyadenosine and 8-3H-deoxyguanosine (using 8-3H-adenine as a labelled DNA precursor) were studied on four isogenic Escherichia coli strains: AB1157 M(+)Y(+) (wild type, mutM(+) mutY(+)), AB1157 M(-)Y(+) (mutM::kan mutY(+) mutant deficient in the formamidopyrimidine-DNA glycosylase MutM), AB1157 M(+)Y(-) (mutM(+) mutY mutant deficient in the A:G mismatch DNA glycosylase MutY), and AB1157 M(-)Y(-) (mutM::kan mutY double mutant deficient in both DNA glycosylases). The main products of transmutation component of 3H decay in position 8 of purine residues are 8-oxo-7, 8-dihydroadenine (8-oxoA) and 8-oxo-7,8-dihydroguanine (8-oxoG), the latter being responsible for the most part of the mutagenic effect. The lethal effects of both gamma-rays and tritium decay virtually did not depend on the repair phenotypes of the host strains used. Therefore, the MutM and MutY glycosylases are not involved in the repair of lethal DNA damages induced by ionizing radiation or by the transmutation component of 3H decay in purine residues of phage DNA. The efficiencies of mutagenic action of 3H-purines E(m) (frequencies of c-mutations per one 3H decay in phage genome) were 2.4-, 3.8- and 55-fold higher in the M(-)Y(+), M(+)Y(-) and M(-)Y(-) mutants, respectively, in comparison to the wild-type host. The mutagenic efficiencies E(m) for gamma-rays were nearly identical in the M(+)Y(+) and M(-)Y(+) hosts, but were increased 1.8- and 8.3-fold, respectively, in the M(+)Y(-) and M(-)Y(-) mutants. These data suggest that: (1) the MutY and MutM DNA glycosylases are important for prevention of mutations caused not only by spontaneous oxidation of guanine residues, but also by ionizing radiation or by decay of 3H incorporated into purine bases of DNA; (2) the MutY and MutM enzymes functionally cooperate in elimination of mutagenic damages induced by these agents.

Bacteriophage lambda↗
PubMed1998

[Lethal and mutagenic effects of tritium incorporated into position 8 of the purines in phage lambda DNA and the role of the Fpg protein].

The lethal and mutagenic effects of the decay of 3H incorporated in phage lambda DNA as 8-3H-adenosine and 8-3H-guanosine were studied, using the DNA of 8-3H-adenine as a labeled DNA precursor. A transmutation component of 3H decay is involved in formation of 8-oxoguanine (8-oxo-G) and 8-oxoadenine (8-oxo-A) residues in phage DNA. The efficiency of phage inactivation (the number of lethal lesions per one tritium decay in the phage genome) for 3H decay in position 8 of purines was the same as that measured in positions 5 and 6 of pyrimidines (alpha = 0.14 +/- 0.01) and virtually did not depend on the fpg-1::kan mutation in the host gene encoding the Fpg protein (formamidepyrimidine-DNA-glycosylase). The efficiency of the mutagenic effect of 3H-purines Em (frequency of c mutations per one 3H decay in the phage genome) was (2.9 +/- 0.3) x 10(-5) in the fpg+ host and (4.6 +/- 0.4) x 10(-5) in the fpg-host. This means that the Fpg protein excised approximately 40% of premutational DNA lesions (probably, 8-oxo-G residues). Induction of the mutagenic SOS system by UV light caused a 1.5-fold increase in the frequency of c mutations induced by 8-3H-purines in fpg+ cells over that in fpg-cells. This suggests that apurinic AP sites produced after the excision of 8-oxo-G by the Fpg protein are substrates for mutagenic SOS repair.

Bacteriophage lambda↗
PubMed1985

[W-mutagenesis in the bisulfite-treated lambda phage].

Survival of phage lambda cI857 inactivated by bisulfite (pH 5.6, 37 degrees C) is higher (the dose modification factor approx. 1.2) and frequency of bisulfite-induced c-mutations 2-4-fold lower on the lawn of the wild-type strain ung+, as compared to ung-1 mutant deficient in uracil-DNA glycosylase. Irradiation of host cells by a moderate UV dose inducing SOS repair system enhances the frequency of bisulfite-induced c-mutations 2-3-fold in the wild-type (ung+) host, but not in the ung-1 mutant. It is suggested that W-mutagenesis in bisulfite-treated lambda phage in the ung+ cells is due to SOS repair of apyrimidinic sites which are produced during excision of uracil residues, the products of cytosine deamination.

Bacteriophage lambda↗
PubMed1981

[Low transfecting efficiency of phage lambda ring chromosomes and their fragments formed by membrane nucleases].

Transfection efficiency of a number of lambda DNA samples differing in ring to linear molecules ratio was determined. Graphic extrapolation to the zero content of linear molecules showed that efficiency of ring molecules did not exceed 5% of that of linear molecules. Probably, this difference is caused by more fast penetration of linear molecules into the cell and, therefore, by lower probability of their degradation by cell wall nucleases. Fragments of both ring and linear molecules formed by cell wall nucleases proved to be inactive in marker rescue experiments.

Bacteriophage lambda↗
PubMed1976

Dependence of transfection efficiency of calcium treated Escherichia coli cells on bacterial genotype and form of Lambda DNA.

The transfecting activity of linear lambda DNA is 100 times higher in calcium treated E. coli K12 (lambda i434) than in non-lysogenic strains: the levels of transfection are 1-2.10(7) and 1-2.10(5) infective centers per 1 mug of lambda DNA respectively. The high efficiency of lysogenic cells transfection is not due to the spontaneously liberated "helper" phage. Evidently, it is called forth by transfecting DNA-prophage recombination or/and by inhibition of nuclease activity in lysogenic cells. Both ring forms lambda DNA (supercoiled and open circles) show very low infectivity, if any, in calcinated cells.

Calcium↗
PubMedDate not supplied

[The lethal and mutagenic action of 3H incorporated into the 2' position of the deoxyribose in the DNA of the extracellular phage lambda].

The lethal and mutagenic effects of 3H decay in 2' position of deoxyribose residues in DNA of extracellular lambda phage were studied, [2'-3H]-deoxyadenosine (3H-dA) or [2'-3H]-thymidine (3H-dT) being used as labelled DNA precursors. As estimated by the efficiency of the lethal and mutagenic actions of 3H decay in position 2' was significantly lower than that of the decay in the incorporated 3H-pyrimidines. The genetic effects of 3H decay in 2' position may be attributed to the radiation effect of beta-particles on DNA. In UV-irradiated E. coli cells, with the induced SOS repair, the mutagenic effect of 3H-dA in phage lambda is significantly higher than that of 3H-dT. This is perhaps related to the formation in DNA of AP-sites, resulting from 3H-decay in 2' position, and to the predominant incorporation of adenosine residues opposite to AP-sites during SOS repair.

Bacteriophage lambda↗
PubMedDate not supplied

[Modification of cellular radiosensitivity by NO-synthase inhibitors].

We recently reported that the treatment of V-79 and HeLa cells with nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) significantly reduced the level of the radiation-induced unstable chromosome aberrations. The stereoisomer D-NAME had no effect. We suggest that the radioprotective effect of L-NAME resulted from the action on the generation reactive radicals due to the inhibition of the NOS-activity. We tested this suggestion on the NO-resistant (ECV-304) and NO-sensitive (HeLa) cells, which were treated with L-NAME or aminoguanidine or D-NAME or cysteamine before gamma-irradiation. There are no significantly differences in radiosensitivity between these cells estimated after exposure by gamma-rays with different doses. However, the radioprotective effect of the NOS-inhibitors manifested only for HeLa. D-NAME had no radioprotective effect neither HeLa nor ECV-304. In contrast NOS-inhibitors, cysteamine treatment EVC-304 reduced the radiation-induced level chromosome aberrations almost twofold. The different mechanisms of the modification of cellular radiosensitivity are discussed.

Chromosome Aberrations↗
PubMedDate not supplied

[Lethal and mutagenic effect of incorporated 6-3H-pyrimidines on extracellular phage lambda].

A study was made of lethal and mutagenic effects of 6-3H-thymidine and 6-3H-cytosine, incorporated into DNA, on extracellular phage lambda. The lethal effects of both 6-3H-pyrimidines (the number of lethal hits per 3H decay) do not differ from those of [3H-methyl]thymidine and 5-3H-cytosine. The mutagenic effects (at equal survival rates) are as follows: 6-3H-thymidine approximately 3H2O less than [3H-methyl]thymidine less than 6-3H-cytosine less than 5-3H-cytosine. UV-irradiation of host cells induces a more pronounced W-mutagenesis with 6-3H-cytosine than with 6-3H-thymidine.

Bacteriophage lambda↗
PubMedDate not supplied

[Lethal and mutagenic action of incorporated 5-3H-cytosine on extracellular phage lambda].

A study was made of the lethal and mutagenic effects on extracellular phage gamma of 5-3H-cytosine incorporated into DNA. The efficiencies of inactivation by incorporated 3H were equal for 5-3H-cytosine and [3H-methyl]-thymidine, but the yield of c-mutations for the former was 14 times higher. The lethal and mutagenic effects of incorporated 5-3H-cytosine did not depend on ung mutation of host cells which caused a deficiency in uracil-DNA-glycosylase. The mutagenic effect was not enhanced when SOS-repair system was induced by UV-radiation. The mutagenic effect of 5-3H-cytosine was associated with the modified mispairing bases but not with uracil residues.

Bacteriophage lambda↗
PubMedDate not supplied

[Lethal and mutagenic activity of tritiated water and incorporated [3H-methyl]-thymidine on extracellular phage lambda].

A study was made of lethal and mutagenic effects on extracellular phage lambda of beta-particles from tritiated water and of [3H-methyl]-thymidine incorporated into DNA. It was shown that the mean lethal dose D10 and the yield of c-mutations per unit of the dose absorbed during external beta-irradiation in 3H2O or during the decay of incorporated [3H-methyl]-thymidine were equivalent to those obtained during 60Co-gamma-irradiation in 4% nutrient broth or at a dried state respectively.

Bacteriophage lambda↗
PubMedDate not supplied

[Infectivity of different forms of lambda bacteriophage DNA in transfection of calcinated Escherichia coli].

Infectivity of linear lambdaDNA molecules is proved to be about a hundred times higher in calcinated E. coli K12 (lambai434) than in E. coli K12(lambda-): the levels of transfection were 1-3-10(7) and 1-2-10(5) infective centers per 1 mug DNA, respectively. In E. coli JC 5743 rec B21 defective for exonucleases I and V the level of transfection was 1-3-10(6). High infectivity of linear lambdaDNA in lysogenic cells cannot be explained by a helping effect of phage particles spontaneously liberated by these cells. It can be caused by recombinations of inserted lambdaDNA molecules with prophage or by the low activity of some nucleases in the lysogenic cells. Covalently closed and "Hershey" ring forms of lambdaDNA penetrate the calcinated cells as readily as linear molecules do but the infectivity of the former ones is proved to be very low.

Coliphages↗
PubMedDate not supplied

[Characterization of the adaptive response to the action of gamma-rays, induced by low doses of 14C in Chinese hamster fibroblasts].

It has been studied the correlation of the mitotic activity of the chromosome aberrations and apoptosis, in the V-79 cells pre-exposure to an adapting dose of ionizing radiation from 14C-thymidine prior to an acute challenge dose of gamma-rays. In spite of that the incubation of the cells with isotope increased of the yield of the chromosome aberrations, but the cells became more resistant to following gamma-irradiation. Increasing the adaptive dose of the 14C on degree didn't influence on the present of the adaptive response. However, using concentrations of the 14C damaged metaphase/anaphase transition and cells blocked in this check-point by apoptotic death. The results suggest, that the cellular selection has been involved in 14C-induced adaptive response, estimated by level of asymmetric chromosome aberrations in V-79 cells.

Adaptation, Physiological↗