[Effect of insertional mutation in the cspA gene encoding the major cold-shock protein on radiation resistance of Escherichia coli]. / Vliianie insertsionnoi mutatsii v gene cspA glavnogo belka kholodovogo shoka na radiorezistentnost' kletok Escherichia coli.

Plasmid pCspA::Km carrying a cloned mutant allele of the cspA gene for the major Escherichia coli cold-shock protein CspA with an insertion of the kanamycin resistance gene cassette from transposon Tn903 into the core region of the coding sequence causes a 2.3-fold increase in radioresistance of wild-type E. coli cells (cspA+). The radioprotective effect of this plasmid is abolished or drastically reduced in mutants recA13 and rpoH15 defective in RecA protein and in induction of the heat-shock protein regulon, respectively. Plasmid pCspA::Km causes a 1.3-fold elevation in the resistance to gamma-irradiation of E. coli mutants with an intermediate level of radioresistance (Gamr445 and KS0160) but slightly diminishes resistance of a highly radiation-resistant Gamr445 mutant. In the chromosome of E. coli with normal DNA repair systems, the cspA::Km mutation in the homozygous state enhances resistance to the lethal effect of gamma-rays and UV light 2.9 and 1.4 times, respectively. These data suggest that the system of cold-shock proteins can modulate resistance of E. coli cells to the lethal effect of gamma-rays and UV light.

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.

[Effect of a null mutation in the priA gene on radioresistance of Escherichia coli]. / Vliianie nulevoi mutatsii v gene priA na radiorezistentnost' Escherichia coli.

According to Kogoma's model of DNA recombination by replication, the PriA protein is involved in the RecBCD pathway of double-strand break (DSB) repair, which is associated with extensive DNA degradation, at the stage of primosome assembly in D-loops (intermediates of strand exchange at the ends of DSB) for the subsequent switch to DSB-induced DNA resynthesis. Comparable data on possible involvement of the PriA protein in the repair of gamma-ray-induced lethal lesions in cells of the wild-type strain of Escherichia coli (strain AB1157) and in two radiation-resistant mutants Gamr445 and Gamr444 were obtained. In all the three strains examined, the null priA2::kan mutation in the structural priA gene was shown to markedly enhance the radiation sensitivity, causing a two- to threefold increase in the slopes of linear dose-survival curves. In the AB1157 strain, the inactivation of PriA is manifested most clearly in the range of low doses (up to 0.15 kGy) when the priA2::kan mutation had only a slight effect on the radiation resistance of Gamr mutants. It can be assumed that, in these mutants with a decreased level of postradiation DNA degradation, the PriA-dependent RecBCD pathway of DSB repair associated with extensive DNA resynthesis is not essential for the repair of lethal lesions at low doses. However, this pathway becomes crucial at higher doses (> 0.5 kGy) even for radiation-resistant strains, especially for the most resistant Gamr444 mutant.

[Constitutive inhibition of DNA degradation due to the enzyme RecBCD in the radiation-resistant Escherichia coli K-12 mutant Gam(r)444]. / Konstitutivnoe ingibirovanie degradatsii DNK, vyzvannoi fermentom RecBCD, u radioustoichivogo mutanta Gam(r)444 Escherichia coli K-12.

Exonucleolytic degradation of [3]H-labeled DNA was examined in partially purified fractions of lysates obtained from nonirradiated RecBCD enzyme-containing cells of Escherichia coli and in the radiation-resistant mutant Gamr444. The degradative activity was shown to be lowered in these cells to the same extent as in the recBC mutant. The efficiency of plating of the mutant phage T4 2-, DNA of which can be degraded by exonuclease V, was 400-fold higher on the strain Gamr444 than on the wild-type strain AB1157. This value was shown to be only twice as low as that on the recB mutant or on the strain AB1157 carrying plasmid pGam26 with a radiation-resistance allele gam26 cloned from mutant Gamr444. The data obtained confirmed the hypothesis that the Gamr444 mutant contains a constitutive inhibitor of exonucleolytic activity of the RecBCD enzyme in nonirradiated cells. This inhibitor was shown to be encoded by the gam26 allele that had previously been mapped at 56.8 min of the E. coli chromosome. A possible mechanism of the involvement of this inhibitor in enhanced radiation resistance of the mutant Gamr444 is considered.

[Natural plasmid pSD89 (Cmr) from Salmonella derby K89, which increases the radiation tolerance of Escherichia coli strain K-12]. / Prirodnaia plazmida pSD89 (Cmr) iz Salmonella derby K89, povyshaiushchaia radioustoichivost' shtammov Escherichia coli K-12.

Several plasmids with molecular mass of 1.3-9 MDa were found in a clinical isolate of Salmonella derby K89 by electrophoresis in agarose gel. One of these plasmids, designated pSD89 (Cmr), was derived from the K89 strain via transformation of the plasmidless recipient S. derby K82 to chloramphenicol resistance. The plasmid-carrying strain K89 and the K82 strain completely cured of plasmids were equally sensitive to the lethal action of UV light, whereas the plasmid-carrying strain was even more sensitive to ionizing radiation than the plasmidless variant. Nevertheless, transformants carrying only plasmid pSD89 (Cmr) were found to be more resistant to gamma-rays and UV light than the recipient. By using an intermediate host Escherichia coli Z80 (r-m+), plasmid pSD89 (Cmr) was introduced into different E. coli K-12 strains: polA-, recA-, uvrA-, umuC-, and the wild-type strain. A slight increase in radioresistance of E. coli wild-type cells and a significant complementation of a repair defect in recA and polA mutants, but not in uvrA and umuC, were observed.

[A mutant allele gam18, participating in the RecF repair path in Escherichia coli K-12]. / Mutantnyi allel' gam18, uchastvuiushchii v RecF-puti reparatsii u Escherichia coli K-12.

Plasmid pGam18 carrying one of the cloned mutant loci, responsible for enhanced radiation resistance in the strain Escherichia coli Gamr444, was shown to increase resistance to the lethal effect of gamma-rays with a dose modification factor DMF = 2. Enhanced resistance was observed in wild-type cells and in the mutant recBC sbcB, but not recFBC sbcA. This indicates the involvement of a product of the gam18 locus in the RecF pathway of recombinational repair. The protective effect of plasmid pGam18 against radiation was completely abolished by mutations in the most RecF pathway genes (recF, recJ, recR, recO, recQ, recN, and ruvB). However, three mutations in the uvrD gene, which encodes DNA helicase II and belongs to the RecF pathway, can be partially complemented by plasmid pGam18. These data suggest that the mutant allele gam18 affects the DNA helicase II activity at the presynaptic stage of the RecF pathway-mediated repair of DNA double-stranded breaks induced by gamma-irradiation.

[Lethal and mutagenic effects of tritium incorporated into position 8 of the purines in phage lambda DNA and the role of the Fpg protein]. / Letal'noe i mutagennoe deistvie tritiia, inkorporirovannogo v 8-e polozhenie purinov v DNK faga liambda, i rol' belka Fpg.

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.

[Hyperrecombination of plasmids is characteristic for hyperresistant strains of Escherichia coli]. / Giperrekombinatsiia plazmid kharakterna dlia giperrezistentnykh shtammov Escherichia coli.

Intraplasmid recombination frequency was assessed in several Escherichia coli K12 strains by the kinetic bioluminescence method. Enhanced plasmid recombination was observed in two mutant E. coli K12 strains, which were hyperresistant to DNA-damaging agents, gamma-rays, photosensitizer 8-methoxypsoralen. Plasmid recombination frequency per one generation (P) was calculated. In mutant strains, this value was shown to exceed that in control isogenic strains with a standard resistance approximately by a factor of 15. Enhanced constitutive synthesis of specific proteins such as heat-shock proteins in Gamr444 and a 55-kDa protein in SA270 in hyperresistant mutant strains is assumed to promote activity of the recombinational RecF pathway system.

[Growth of radiation resistance in bacteriophages as a result of intensifying expression of the stress system in host cells]. / Rost radioustoichivosti bakteriofagov kak rezul'tat usileniia ékspressii stressovykh sistem kletki-khoziaina.

By means of polyacrylamide gel electrophoresis (PAGE) of proteins from radiation-resistant Gamr mutants of Escherichia coli, it was shown that induction and elimination of RecA protein in these mutants are kinetically more rapid than in wild type cells, and heat-shock proteins (HSP) are hyperproduced even at a normal temperature (32 degrees C). gamma-and UV-irradiated bacteriophages were used to study the results of simultaneous enhanced expression of two stress repair systems. Radiation-resistant mutants are similar to wild type cells in their ability to reactivate phages lambda CI, phi 80 vir, and T 4D inactivated by gamma-rays and UV-light. W-reactivation of gamma-irradiated phages lambda and 80 vir is respectively 1.5 and 1.2 times higher in Gamr cells in which maximal w-reactivation was observed at wide range of doses (from 300 to 2000 Gy) whereas in wild type cells the peak of W-reactivation was registered at doses of 400 to 450 Gy. The phage lambda gamma-, irradiated upon adsorption on the cells of a radiation-resistant mutant, was two times more resistant to gamma-rays (DMF = 2 at LD10) than when irradiated upon adsorption on wild type cells. Postirradiation degradation of the phage lambda DNA, when irradiated within Gamr cells, was significantly lower than in wild type cells, and preirradiation of the cells decreased phage DNA degradation (12% in Gamr cells and 30% in wild-type cells). The role of an increased HSP level and expression of SOS-regulon in radiation resistance and possible interaction of stress systems in bacterial cells are discussed.

[Mutagenic effect of oxidizing agents on the thermally-induced prophage lambda cI857: effect of a system of oxidative stress]. / Mutagennoe deistvie okislitel'nykh agentov na termoindutsiruemyi profag lamdacI857: vliianie sistemy okislitel'nogo stressa.

The lethal and mutagenic effects of hydrogen peroxide H2O (2-20 mM), cumene hydroperoxide (0.2-2.0 mM), and potassium permanganate KMnO4 (0.25-1.0 mM) on the heat-inducible lambda cI857 prophage were studied under conditions of heat-induction immediately after the mutagenic treatment of lysogenic cells of Escherichia coli oxyR+ or oxyR delta 3. Within the range of the doses used, these agents decreased prophage survival by 3-5 orders of magnitude and increased mutation frequency by up to 0.2% under the action of hydrogen peroxide and cumene hydroperoxide, and up to 1.5% in the case of KMnO4 (in oxyR+ cells). In the absence of the inducible OxyR system of oxidative stress, both lethal and mutagenic effects of H2O were enhanced. The oxyR delta 3 mutation increased lethal and mutagenic effects of cumene hydroperoxide and KMnO4 only at the highest concentrations used. Apparently, the OxyR system does not repair lesions induced by oxidative agents, but only prevents their formation.

[Mutant alleles for radioresistance form the Escherichia coli strain Gam(r)444): cloning and preliminary characteristics]. / Mutantnye alleli radiorezisteentnosti iz shtamma Escherichia coli Gam(r)444: klonirovanie i predvaritel'naia kharakteristika.

Mutant alleles Gamr, which are able to increase the resistance to radiation of Escherichia coli wild-type cells, were cloned from the hyperradioresistant mutant Gamr444 on a plasmid mini-Mu vector MudII4042. The influence of recombinant plasmids on the sensitivity of wild-type and mutant (recA and htpR) cells to gamma-irradiation was studied. It was shown that the enhanced resistance of the Gamr444 strain to radiation was caused by mutations of two different classes, dominant and recessive. The cloned recessive mutation gamr12 increases resistance to radiation only after homogenization, that is, radiation-induced transfer from the plasmid to the chromosome, and it imposes constitutive expression of the heat-shock promoter htpG. Dominant mutant gamr alleles are active in the trans-position. A mutation-insertion into a chromosomal gene impaired by one of the dominant mutations, gamr18, was constructed. The insertion causes drastic cell radiosensitization on the recB sbcB background and probably disturbs the RecF pathway of recombination and repair. Dominant plasmids of the second type lead to the RecA-independent inhibition of DNA postirradiation degradation. The radioprotective action of recessive and dominant gamr mutations is additive.

[Induction of the SOS-like system in Rec-mutants of Bacillus subtilis]. / Induktsiia SOS-podobnoi sistemy u Rec-mutantov Bacillus subtilis.

Influence of the recE1, recB2, recB3, recB19, recF15, recF18, recL16, recM13 and recM27 mutations of the induction of the SOS-like system component, i. e. the RecE protein of Bacillus subtilis was studied by RIA-dot-blot method in UV-irradiated or treated by nalidixic acid cells. These agents caused a significant increase in the wild type (rec+) cells but did not stimulate the RecE synthesis in the rec mutants tested. The two exceptions were recB2 and recF18 mutants treated by nalidixic acid. The tsi23 mutation caused thermoinduction of phi 105 bacteriophage in the rec+ genetic background while no prophage particles were induced in the recE, recF, recL, recM mutants. The data suggest that the genetic damage of several rec genes including recB, recE, recF, recL and recM can block induction of the SOS-like system of Bacillus subtilis.

[The lethal and mutagenic action of 3H incorporated into the 2' position of the deoxyribose in the DNA of the extracellular phage lambda]. / Letal'noe i mutagennoe deistvie 3H, inkorporirovannogo v polozhenie 2' dezoksiribozy v DNK vnekletochnogo faga 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.

[The adaptive response to mitomycin C exposure in the hyper-radioresistant mutant Escherichia coli Gamr444]. / Adaptivnyi otvet na vozdeistvie mitomitsinom C u giperradiorezistentnogo mutanta Escherichia coli Gamr444.

Adaptive response to mitomycin C (MC) (lethal effect and recovery of molecular mass of DNA) in hyper-radioresistant mutant Escherichia coli Gamr444 have been investigated. This mutant is more resistant to MC than parent strain E. coli K12 AB1157. Adaptation of Gamr444 mutant to MC in nonlethal concentrations increases its resistance to MC in lethal concentrations with dose modification factor (DMF) 2.4 at the LD90 level. During the adaptation of this mutant to methyl-methane sulfonate (MMS) its resistance to this agent increases with DMF by 2.2 and resistance to MC with DMF by 1.5 times. During the adaptation of Gamr444 mutant to MC its resistance to MMS increases with DMF by 1.5 times. Adaptive response to MC abolishes by chloroamphenicol treatment during the adaptation. Adaptive response to nitrogen mustard (HN2) in E. coli Gamr444 is absent (HN2 induces cross-links in DNA as MC). Degradation of DNA following the formation of cross-links in DNA takes place. Adaptation to MC in Gamr444 mutant leads to restoration of DNA molecular mass which is more quicker than in the case without adaptation. Adaptive restoration of DNA molecular mass after the MC treatment is absent in E. coli K12 AB1157. The repair of cross-links in DNA after the treatment of HN2 in Gamr444 mutant takes place with equal rate both in the case of adaptation to HN2 and in the case without adaptation. It is proposed, that under the treatment of MC in E. coli Gamr444 the ada-alkA-dependent adaptive response takes place. This adaptive response is connected with alkylation of O6-guanine and elimination of the product by O6-alkyl-DNA-alkyltransferase. Partial recA-dependency of the adaptive response to MC allows to suggest the participation of another inducible system. The nature of this system is unknown.

[Lethal and mutagenic effect of incorporated 6-3H-pyrimidines on extracellular phage lambda]. / Letal'noe i mutagennoe deistvie inkorporirovannykh 6-3H-pirimidinov na vnekletochnyi fag 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.

[Mutants of Escherichia coli K-12 with increased resistance to ionizing radiation. VI. Increased radioresistance and heat shock proteins]. / Mutanty Escherichia coli K-12 s povyshennoi ustoichivost'iu k ioniziruiushchei radiatsii. Soobshchenie VI. Povyshennaia radiorezistentnost' i belki teplovogo shoka.

By means of one-dimensional electrophoresis, it is shown that in radiation-resistant Gamr444 and Gamr445 mutants of Escherichia coli K-12 high-molecular weight heat shock proteins are hyperproduced at 32-37 degrees C and are induced more intensively during heat shock (in comparison to the parental wild-type strain AB1157). When the missense htpR15 mutation of the positive regulatory htpR gene for heat shock proteins was introduced by transduction into the genome of the Gamr444 mutant, its enhanced radiation-resistance disappeared but could be restored upon introduction of pKV3 plasmid bearing the htpR+ gene. These data show that heat shock proteins are participating in the enhanced radioresistance of Gamr mutants.

[Thermoinduced radioresistance of Escherichia coli cells and heat shock proteins]. / Termoindutsirovannaia radiorezistentnost' kletok Escherichia coli i belki teplovogo toka.

Radioresistance of E. coli cells is slightly increased (dose modification factor (DMF) = 1.2) with temperature elevated from 4 degrees to 43 degrees C at the time of gamma-irradiation. However, an appreciable effect of the thermoinduced radioresistance (DMF = 1.7) was observed when the wild-type cells were exposed to gamma-radiation at 15-43 degrees C (but not at 4 degrees C) after 30-min preincubation at 43 degrees C. This effect was absent in htpR mutants, defective in induction of heat shock proteins, and coupled with the decreased post-irradiation DNA degradation in gamma-irradiated htpR+ cells. It is suggested that heat shock proteins are involved in the thermoinduced radioresistance.

[W-mutagenesis in the bisulfite-treated lambda phage]. / W-mutagenez u faga liambda, obrabotannogo bisul'fitom.

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.

[Mutagenic effect of o-methylhydroxylamine on the prophage and extracellular phage lambda]. / Mutagennoe deistvie o-metilgidroksilamina na profag i vnekletochnyi fag lambda.

Induction of c-mutations in extracellular bacteriophage and prophage lambda cI857 ind-treated with 1 M O-methylhydroxylamine (OMHA) at 32 degrees and pH 5.6 has been studied. The frequency of c-mutations increases proportionally to the time of treatment of extracellular phage and does not depend on cellular recA+ or polA+ functions and on induction of SOS-repair system caused by UV-irradiation of host cells. Prophage is inactivated and mutagenized approximately 10-fold faster than extracellular phage immediately after treatment of lysogenic cells during prophage induction. Thus, prophage survival does not depend on repair functions of the host cells, and the frequency of c-mutations in recA and, especially, in polA lysogens is significantly lower, than in the wild-type cells. Delayed thermoinduction (90 min) of prophage causes significant enhancement of survival and decreases the frequency of c-mutations in all strains studied. Preliminary treatment of non-lysogens with OMHA does not increase the frequency of c-mutations in undamaged phage or in phage treated with OMHA in vitro.

[Lethal and mutagenic action of incorporated 5-3H-cytosine on extracellular phage lambda]. / Letal'noe i mutagennoe deistvie inkorporirovannogo 5-3H-tsitozina na vnekletochnyi fag lamda.

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.