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M Sedliaková

Publications and source records attributed to M Sedliaková.

At least 19 recordsLinked to original sources
PubMed2000

Inducible stable DNA replication (iSDR) and the uvr-dependent tolerance of pyrimidine dimers in UV-irradiated Escherichia coli are two uncoupled processes.

Inducible stable DNA replication (iSDR) is dependent on recombination and is supposed to play a role in DNA repair of Escherichia coli. Our previous data suggested that iSDR may be involved in the tolerance of UV lesions, which remain unexcised in excision-proficient E. coli exposed to some UV pretreatments. Now, the tolerance of unexcised lesions has been followed in E. coli recB21 and in E. coli priA1 sup mutants, incapable of iSDR. The obtained data do not confirm the previous hypothesis about the involvement of iSDR in the putative uvr-dependent lesion tolerance. They rather suggest that iSDR and the uvr-dependent lesion tolerance are two uncoupled processes.

DNA Repair↗
PubMed1997

The effect of the OmpT protease on excision repair in UV-irradiated Escherichia coli.

The extent of pyrimidine dimer excision (PDE) was inhibited in UV-irradiated E. coli KS272 (ompT+) cells when they were preinduced by a low UV predose preceded by a nutrition stress but not in the preinduced E.coli SF100 (ompT-) mutants. The preinduction, however, markedly inhibited PDE in the ompT- cells transformed with a multicopy plasmid carrying ompT gene. The data are consistent with the hypothesis that the inducible OmpT protease (controlled by rpoH) might terminate the SOS period of excision repair so that when cells are preinduced PDE might be inhibited prematurely.

DNA Damage↗
PubMed1996

Constitutive increase of RecA protein: its influence on pyrimidine dimer excision and survival of UV-irradiated Escherichia coli.

Transformation of E. coli with the plasmid pRA containing recA gene increased the constitutive level of RecA protein 50-67 fold. This slightly inhibited pyrimidine dimer excision and reduced cell survival in three investigated, UV-irradiated E. coli strains. Our data support the view that RecA protein prematurely present at a high level may mask the dimers. The masking subsequently reduces the dimer excision and switches off the inducing signal.

DNA, Bacterial↗
PubMed1995

Inducible stable DNA replication of Escherichia coli tolerates unexcised pyrimidine dimers in an uvr-dependent manner.

Damage-inducible DNA replication (iSDR) was followed in UV-irradiated E. coli uvr+ and uvr B5 cells. Owing to the inhibition of dimer excision in the former (caused by the metabolic treatment), both contained similar amounts of unexcised dimers. Since the iSDR took place in uvr+ but not in uvr B5 cells, it is concluded that the uvr system can tolerate unexcised dimers through the recombinogenic iSDR.

DNA Damage↗
PubMed1995

DNA repair in Escherichia coli: the dual function of uvr genes.

It has been shown earlier that the starvation of E. coli for both amino-acids and thymine applied prior to UV irradiation inhibits pyrimidine dimer excision without affecting cell survival after UV irradiation. In such cells pyrimidine dimers are tolerated by a rather error-free process that depends on the activity of uvrB, recA and lexA genes. Data presented here show: (a) that the efficient toleration of unexcised dimers requires also the uvrA gene; (b) that the starvation increases the level of RecA protein about 4.7 times; (c) that the effect of starvation on subsequent pyrimidine dimer excision is reversed by a 2 h incubation in complete medium before the cells are UV irradiated. The data suggest that the uvrA, uvrB, recA, lexA dependent nonexcisional repair may be a pathway temporarily functioning in repeatedly damaged cells.

Adenosine Triphosphatases↗
PubMed1993

Inhibition of dimer excision in repeatedly UV-irradiated Escherichia coli: its requirement for RecA protein and de novo protein synthesis.

In UV-irradiated Escherichia coli dimer excision was found to be inhibited by predamage (M. Sedliaková, F. Masek and J. Brozmanová, FEBS Lett., 23 (1972) 325-326) or overproduction of RecA protein, which suggests that the coating of the dimers by this protein may make them inaccessible to the excision nuclease (M. Sedliaková, K. Kleibl and F. Masek, Mutat. Res., 191 (1987) 13-16). We measured the levels of RecA protein and dimer excision in cells irradiated with (i) a single dose of 50 J m-2, (ii) two separate doses of 30 and 50 J m-2, post-incubated with chloramphenicol; (iii) two separate doses of 30 and 50 J m-2, post-incubated without chloramphenicol. Dimer excision was complete in the first two cases, but in the latter it was inhibited by 40%. At the time of active dimer excision, there were marked differences in RecA protein content between the cells irradiated with a single dose and cells irradiated with two separate doses (both post-incubated without chloramphenicol), which might account for the differences in dimer excision. However, relatively small differences in RecA protein content were found in cells irradiated with two doses and post-incubated with or without chloramphenicol, which could therefore not account for the differences in dimer excision. The data suggest that the inhibition of dimer excision involves some short-lived component(s) other than RecA protein.

Bacterial Proteins↗
PubMed1993

UmuC product contributes to the inhibition of dimer excision produced by thymine-less-amino acid-less pretreatment in UV-irradiated Escherichia coli.

In UV-irradiated Escherichia coli, predamaged by thymine-amino acid starvation or a UV predose, a large amount of dimers may remain unexcised and may be tolerated by an error-free mechanism, which requires the function of uvr, recA and lexA genes. A possible role of the umuC gene in both the inhibition of dimer excision and the toleration of unexcised dimers is investigated. Data suggest that the UmuC gene product is not absolutely necessary for the inhibition of dimer excision in UV-irradiated thymine-less-amino acid-less pretreated cells, but that it contributes to it. However, the UmuC product does not seem to be involved in the toleration of unexcised dimers which is dependent on uvr, recA and lexA.

Bacterial Proteins↗
PubMed1992

Effect of plasmid pKM101 in ultraviolet irradiated uvr+ and uvr- Escherichia coli.

The effect of plasmid pKM101 on UV irradiated excision proficient and excision deficient cells was investigated. The plasmid increased the survival of excision proficient cells while partially inhibiting thymine dimer excision. The frequency of mutations was almost unchanged. In excision deficient cells the effect of the plasmid on survival was less pronounced while cell mutability was increased. Our data indicate that the mucAB genes (carried by the plasmid) influence the two types of cells in a different way.

DNA Repair↗
PubMed1992

Inducible stable DNA replication in Escherichia coli uvr+ and uvr- cells, treated with genotoxic chemicals.

Inducible stable DNA replication (iSDR) provoked by a damaging treatment with MMS, MNU, MNNG, NFAA, NFN, 4NQO, NAL or MMC, was followed in both repair-competent E. coli PQ35 and its uvrA derivative E. coli PQ37. In contrast to SOS-inducible mutagenesis, which is more pronounced in excision-deficient cells, iSDR was more obvious in repair-competent cells. This may be due to special features of iSDR and need not indicate involvement of the uvrA gene product in it.

4-Nitroquinoline-1-oxide↗
PubMed1991

uvrB-dependent, recF-independent post-replication (or replication) repair in Escherichia coli.

In UV-damaged cells, a large fraction of pyrimidine dimers may remain unexcised and may be tolerated by a uvrB recA lexA-dependent non-excisional mode of repair (M. Sedliaková, J. Brozmanová, F. Maŝek and K. Kleibl, Biophys. J., 36 (1981) 429-441). We show here that a similar repair pathway operates in the Escherichia coli recF 143 single mutant but not in the recF uvrB double mutant. This indicates that the putative repair pathway is recF independent.

Bacterial Proteins↗
PubMed1989

Repression of damage-inducible (din) genes by the lexA3 mutation or by plasmid carrying the lexA gene; effect on pyrimidine dimer excision in UV-irradiated Escherichia coli.

Dimer excision was followed in Escherichia coli K-12 AB1157 DM49 lexA3 mutant (whose repressor is not cleavable with RecA protease), and in E. coli K-12 AB2497[pGC3] carrying the cloned lexA gene. In either case din genes could not be efficiently derepressed. In such cells ultraviolet (UV) irradiation caused an extensive DNA degradation, which was not observed in cells with derepressed din genes. Even after a high UV dose (70 J/m2) dimers were being excised efficiently. However, progressive DNA degradation interfered with the precise detection of unexcised dimers. We conclude that induction of din genes is required for filling some of the gaps and for prevention of DNA degradation, but not for excision itself.

Bacterial Proteins↗
PubMed1989

In UV-irradiated Escherichia coli PQ35 overproducing the RecA protein, expression of the sfiA gene and dimer excision are alleviated.

Escherichia coli PQ35 cells carrying the sfiA-::lacZ operon fusion were transformed either with a multicopy plasmid containing the recA gene (pHSG262 recA) or with a multicopy plasmid alone (pHSG262). Both transformants were UV irradiated. Then induction of the sfiA gene and dimer excision were followed. Amplification of the recA gene partly inhibited both sfiA gene induction and dimer excision. The following interpretation of this phenomenon is proposed. When the RecA protein is in abundance, pyrimidine dimers are quickly masked by it. The masked dimers are less efficiently distinguished by excision nuclease and do not provide the induction signal. Due to this, induction of the sfiA gene as well as dimer excision are inhibited early.

Bacterial Proteins↗
PubMed1987

Inhibition of pyrimidine dimer excision in ultraviolet-irradiated Escherichia coli overproducing RecA protein.

Escherichia coli Br Hcr+ cells transformed with the recombinant multicopy plasmid pBR322 carrying recA gene contain increased amounts of RecA protein. When these cells were UV-irradiated, excision of pyrimidine dimers was reduced by about 50%. It is suggested that the damaged DNA strands may be coated with RecA protein which makes them insensitive to the action of the uvrABC excision nuclease.

DNA Repair↗
PubMed1984

DNA of Chinese hamster V79 cells newly synthesized after ultraviolet irradiation contains alkali-labile sites.

Pulse-labeled daughter DNA of UV-irradiated Chinese hamster V79 cells was denatured in alkaline or neutral conditions and analysed by sucrose gradient centrifugation. A comparison of the sedimentation profiles of DNA treated in alkaline or neutral conditions has shown that in UV-irradiated cells some alkali-labile sites are produced during replication of damaged templates.

Alkalies↗
PubMed1984

Error-free uvr+-dependent inducible DNA repair in Escherichia coli B/r Hcr+ cells.

The frequency of suppressor (tryptophan reversions) and of true (streptomycin-resistant and dependent) mutations has been followed in E. coli cells irradiated with a single dose or two separate doses of ultraviolet (U.V.) radiation. Under these conditions dimers were efficiently excised after a single dose, while about 40 per cent of the dimers remained unexcised after two doses. Although the level of unexcised dimers in the latter case increased proportionally with the second U.V. dose, the mutation frequency increased by 1.5-2-fold, but did not continue to increase with the level of unexcised dimers. A comparison of excision-proficient and excision-deficient cells containing similar amounts of persisting dimers has shown that proficient cells can tolerate a high level of dimers without an adequate increase in mutation frequency. Our results suggest the existence of an error-free uvr+-dependent inducible repair in E. coli B/r Hcr+ cells.

Cell Survival↗