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F Masek

Publications and source records attributed to F Masek.

At least 37 records · Page 2Linked to original sources
PubMed1981

Evidence that dimers remaining in preinduced Escherichia coli B/r Hcr+ become insensitive after DNA replication to the extract from Micrococcus luteus.

In Escherichia coli B/r Her+ irradiated with two separate fluences, dimer excision is prematurely interrupted. The present study was designed to follow tha fate of dimers remaining unexcised. The results imply that these dimers (or distortions containing dimers) are transformed on replication from the state of sensitivity to the state of insensitivity to endonuclease from Micrococcus luteus. This conclusion is based on the following findings: (a) dimers were radiochromatographically detectable in DNA replicated after UV, which indicated that they were tolerated on replication. (b) Similar amounts of dimers were detected radiochromatographically both in DNA remaining unreplicated and DNA twice replicated after UV, This along with the low transfer of parental label into daughter DNA, indicated that dimers remained in situ in parental chains. (c) Immediately after UV, all parental DNA contained numerous sites sensitive to the extract from M. luteus. 2 h after UV, a portion of parental DNA still contained a number of endonuclease-sensitive (Es) sites, while another portion of parental DNA and all daughter DNA were free of Es sites. (d) The occurrence of parental DNA free of Es sites was not temporally correlated with dimer excision, but with the first round of DNA replication. (e) The amount of DNA free of Es sites corresponded to the amount of replicated DNA. (f) Separation of replicated and unreplicated DNA, and detection of Es sites in both portions separately showed that the replicated DNA was almost free of Es sites, whereas unreplicated DNA contained a number of such sites.

DNA Replication↗
PubMed1978

UV-inducible repair: influence on survival, dimer excision, DNA replication and breakdown in Escherichia coli B/r Her+ cells.

Using a model of double-UV-irradiation with inducing1 (non-lethal) and lethal fluences2 we have studied involvement of UV-inducible functions in post-UV-irradiation restoration processes and survival of Escherichia coli B/r thy-trp-Hcr+. Cells irratiated with both inducing and lethal fluences differed from cells irradiated with lethal fluence in the following respects: They were more UV resistant; they did not die during postincubation with chloramphenicol3; they exhibited a significant reduction in dimer excision; they were able to resume DNA replication and produce normal-sized DNA molecules in the presence of chloramphenicol. Since induction was provoked in cell prestarved for amino acids it was not associated with damage to points active in replication. However, the inducible product was more important for repair of replicating than non-replicating cells. The data indicate that protein necessary for resumption of DNA synthesis after UV is not constitutive but inducible.

DNA Repair↗
PubMed1977

Dependence of DNA dark repair on protein synthesis in Escherichia coli.

We investigated the influence of amino-acidless treatments applied prior and after UV irradiation (AA-irradiated AA+; AA-irradiated A-; AA+ irradiated AA-) on survival, dimer excision, postirradiation DNA degradation, DNA synthesis and sedimentation profiles of parental DNA of E. coli B/r Hcr+ cells. In dependence on the treatment applied, the fluence 50 J/m2 yielded distinctly different fractions of survivors within 0,03-85%. In all cases dimers were completely excised. The rate of DNA degradation was similar during a 30-40 min period after UV during which the bulk of dimers was excised. Degradation ceased, however, earlier in the prestarved cells than in exponentially growing ones; it was prolonged by aminoacidless postincubation. Sedimentation profiles of parental DNA did not differ during the whole period of dimer excision. In AA+ AA- cells DNA synthesis was not restored for several hours after addition of amino acids. In AA- AA- cells addition of amino acids resulted in a fast resumption of DNA synthesis. We conclude that removal of dimers and repair of gaps were similar in all cases. We believe that aminoacidless treatments influence production and repair of damage to the sites of DNA replication. The treatment appears to prevent this damage when applied before UV irradiation, but interferes with its restoration when applied after UV irradiation. Consequently, the former treatment increases survival of cells while the latter produces an opposite effect.

Amino Acids↗
PubMed1977

Effect of some drugs on excision repair in E. coli cells.

The intercalating dye ethidium bromide (EB), inhibits excision of pyrimidine dimers from UV-irradiated excision-proficient Escherichia coli B/r hcr+ cells. Inhibition is total at a 2.5 - 10(-4) M concentration 120 min after irradiation with a dose of 750 erg/mm2. The viability of irradiated cells diminishes in proportion to the EB concentration. Under wholly analogous conditions of cultivation and irradiation no inhibitory effect of KCN and caffeine (CFF) and only a slight effect of chloramphenicol (CAP) on dimer excision has been observed. The viability of cells is affected by these compounds but it does not appear to depend on the quantity of excised photoproducts. A change in the secondary structure of DNA induced by intercalation of EB appears to be the reason for the depression of excision of UV photoproducts.

Caffeine↗
PubMed1975

Comparison of the effect of nalidixic acid and thymine deprivation on excision repair in Escherichia coli.

There is a difference in the extent of inhibition of thymine dimers (TT) excision in ultravioley (UV) irradiated cells of E. coli after preirradiation depression of protein and DNA syntheses induced by a simultaneous deprivation of essential amino acids (AA-) and thymine(T-) or by deprivation of essential amino acids and addition of nalidixie acid (NAL+). This difference has been noted in both E. coli B/r Her+ and E. coli K12 SR20 uvr+ cells. Depression of DNA synthesis with the aid of malidixic acid as exogenous agent will inhibit TT excision to a lesser degree than depression of DNA synthesis by thymine starvation. The extent of TT excision has no appreciable influence on restoration of the sedimentation profile of newly synthesized DNA nor again on UV resistance of cells in conditions of dark repair. At the time when there are TT still present in DNA, the DNA molecule, having the size of the molecule of unirradiated cells, will become synthesized.

DNA Repair↗
PubMed1975

Function of the UVR marker in dark repair of DNA molecules.

It had been found earlier that the excision repair mechanism in E. coli B/R Hcr+ could be depressed by preirradiation, amino acid and thymine starvation; such an interference proved to have no appreciable influence on survival after ultraviolet irradiation. A comparison between Hcr+ and Hcr- cells had revealed that the former were capable of tolerating a greater amount of unexcised dimers than the latter. In this paper it is demonstrated that the above-mentioned pretreatment will depress excision activity also in cultures of E. coli K12 and E. coli 15T- both strains of the uvr+ rec+ genotype. A comparison of two E. coli K12 strains of the uvr+ and uvr- genotype shows that uvr+ cells also have a greater capacity to tolerate unexcised dimers. To throw light on the nature of that increased capacity to tolerate unexicsed dimers we have compared restoration of DNA daughter chains in cells of the uvr+ and uvr- genotype and found that integrity of uvr loci is a conditio sine qua non for an effective restoration of daughter chains, but that depression of excision activity by the mentioned pretreatment does not influence restoration of DNA daughter chains. This suggest that uvr loci are involved not only in excision but also in postreplication mechanism of DNA repair.

DNA Repair↗