Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deoxyribonucleic acid polymerase I-directed repair synthesis can be selectively measured in toluene-treated Escherichia coli cells exposed to alkylating chemicals such as N-methyl-N'-nitro-N-nitrosoguanidine. Prior growth of the cells in the presence of a low dose of N-methyl-N'-nitro-N-nitrosoguanidine results in an enhanced deoxyribonucleic acid polymerase I-directed repair synthesis and an increase in single-strand breaks.
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PMID:Enhancement of deoxyribonucleic acid polymerase I-directed repair synthesis in toluene-treated Escherichia coli after growth in the presence of low levels of N-methyl-N'-nitro-N-nitrosoguanidine. 37 53

Initiation of new DNA synthesis was observed in B. subtilis cells upon gamma-ray irradiation followed by toluene treatment and incubation in the presence of the four deoxynucleotide triphosphates and Mg2+. This DNA synthesis took place in the absence of ATP and was refractory to 6-(p-hydroxyphenylazo)-uracil which is a specific inhibitor for the type III polymerase of Bacillus subtilis. This repair-type DNA synthesis was greatly reduced in mutant cells deficient in DNA polymerase I. Restoration of transforming activity of cellular DNA was found to occur in parellel with the above repair type DNA synthesis. A protein factor which enhances the priming activity of gamma-irradiated DNA for DNA polymerase I was detected in DNA-free extracts prepared from B. subtilis cells by means of lysis with a buffer containing lysozyme, Brij-58 and EDTA.
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PMID:Studies on DNA repair in Bacillus subtilis. I. A cellular factor acting on gamma-irradiated DNA and promoting its priming activity for DNA polymerase I. 80 54

Ultraviolet irradiation of toluene-treated Escherichia coli causes an inhibition of replicative DNA synthesis. This is followed by the appearance of nonconservative DNA repair synthesis which does not require either the polymerase or 5' leads to 3' exonucleolytic activities of DNA polymerase I. The repair synthesis may be catalyzed by DNA polymerase III activity but does not require a functional DNA polymerase II. The ultraviolet-induced synthesis requires ATP and is dependent on a functional uvrA and uvrB gene product. However, other uvr gene products are not required for the synthesis. The recB function is also not required.
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PMID:DNA repair synthesis dependent on the uvrA,B gene products in toluene-treated cells. 110 Jun 28

We have examined the modes of DNA synthesis in Escherichia coli strains made permeable to nucleoside triphosphates by treatment with toluene. In this quasi in vitro system, polymerase-I-deficient mutants exhibit a nonconservative mode of synthesis with properties expected for the resynthesis step of excision-repair. This UV-stimulated DNA synthesis can be performed by either DNA polymerase II or III and it also requires the uvrA gene product. It requires the four deoxynucleoside triphosphates; but, in contrast to the semiconservative mode, the ATP requirement can be partially satisfied by other nucleoside triphosphates. The ATP-dependent recBC nuclease is not involved. The observed UV-stimulated mode of DNA synthesis may be part of an alternate excision-repair mechanism which supplements or complements DNA-polymerase-I-dependent repair in vivo.
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PMID:Repair replication in permeabilized Escherichia coli. 110 30

Toluene-treated cells were used for examining excision of pyrimidine dimers in Escherichia coli strains W3110, DM845 (uvrA-), P3478 (polA-), and KS5064 (polAex1). Excision occurring in toluene-treated cells is rapid, adenosine 5'-triphosphate dependent, and requires the uvrA gene function. In strains lacking either the polymerizing or 5' leads to 3' exonucleolytic activity of deoxyribonucleic acid polymerase I, excision does occur. However, both in vivo and in vitro, the excision in such strains is initially slower than wild type.
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PMID:Excision of pyrimidine dimers in toluene-treated Escherichia coli. 110 6

The repair response of Escherichia coli to hydrogen peroxide-induced DNA damage was investigated in intact and toluene-treated cells. Cellular DNA was cleaved after treatment by hydrogen peroxide as analyzed by alkaline sucrose sedimentation. The incision step did not require ATP or magnesium and was not inhibited by N-ethylmaleimide (NEM). An ATP-independent, magnesium-dependent incorporation of nucleotides was seen after the exposure of cells to hydrogen peroxide. This DNA repair synthesis was not inhibited by the addition of NEM or dithiothreitol. In dnaB(Ts) strain CRT266, which is thermolabile for DNA replication, normal levels of DNA synthesis were found at the restrictive temperature (43 degrees C), showing that DNA replication was not necessary for this DNA synthesis. Density gradient analysis also indicated that hydrogen peroxide inhibited DNA replication and stimulated repair synthesis. The subsequent reformation step required magnesium, did not require ATP, and was not inhibited by NEM, in agreement with the synthesis requirements. This suggests that DNA polymerase I was involved in the repair step. Furthermore, a strain defective in DNA polymerase I was unable to reform its DNA after peroxide treatment. Chemical cleavage of the DNA was shown by incision of supercoiled DNA with hydrogen peroxide in the presence of a low concentration of ferric chloride. These findings suggest that hydrogen peroxide directly incises DNA, causing damage which is repaired by an incision repair pathway that requires DNA polymerase I.
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PMID:Repair response of Escherichia coli to hydrogen peroxide DNA damage. 353 65

The thymidine analog 3'-azido-3'-deoxythymidine (BW A509U; azidothymidine [AZT]) had potent bactericidal activity against many members of the family Enterobacteriaceae, including strains of Escherichia coli, Salmonella typhimurium, Klebsiella pneumoniae, Shigella flexneri, and Enterobacter aerogenes. AZT also had bactericidal activity against Vibrio cholerae and the fish pathogen Vibrio anguillarum. AZT had no activity against Pseudomonas aeruginosa, gram-positive bacteria, anaerobic bacteria, Mycobacterium tuberculosis, nontuberculosis mycobacteria, or most fungal pathogens. Several lines of evidence indicated that AZT must be activated to the nucleotide level to inhibit cellular metabolism: AZT was a substrate for E. coli thymidine kinase; spontaneously arising AZT-resistant mutants of E. coli ML-30 and S. typhimurium were deficient in thymidine kinase; and intact E. coli ML-30 cells converted [3H]AZT to its mono-, di-, and triphosphate metabolites. Of the phosphorylated metabolites, AZT-5'-triphosphate was the most potent inhibitor of replicative DNA synthesis in toluene-permeabilized E. coli pol A mutant cells. AZT-treated E. coli cultures grown in minimal medium contained highly elongated cells consistent with the inhibition of DNA synthesis. AZT-triphosphate was a specific DNA chain terminator in the in vitro DNA polymerization reaction catalyzed by the Klenow fragment of E. coli DNA polymerase I. Thus, DNA chain termination may explain the lethal properties of this compound against susceptible microorganisms.
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PMID:Antibacterial activity and mechanism of action of 3'-azido-3'-deoxythymidine (BW A509U). 355 32

Ultraviolet (UV)-stimulated nonconservative DNA synthesis has been observed in E. coli rendered permeable to nucleoside triphosphates by exposure to toluene. This synthesis is detected in toluenized cells in which the background of UV-independent DNA synthesis is reduced by use of dnaB mutants temperature-sensitive for DNA replication and additionally deficient in DNA polymerase I. UV-stimulated nonconservative synthesis is also seen in polA dnaE mutants that are deficient in two of the three known DNA polymerases. The observed UV-stimulated repair-like synthesis requires the presence of the four deoxyribonucleoside triphosphates and ATP. This mode of synthesis appears to differ from the ATP-independent nonconservative DNA synthesis previously reported to occur in toluenized bacteria.
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PMID:Ultraviolet-stimulated DNA synthesis in toluenzied Escherichia coli deficient in DNA polymerase I. 456 30

Deoxyribonucleoside triphosphates are incorporated into T4 DNA in infected cells treated with toluene. Under the proper conditions the incorporation is controlled by the known T4 DNA polymerase and proceeds by a semiconservative mechanism. Both strands of the phage DNA are replicated into a high molecular weight progeny molecule. The replication system is accessible to extracellular pancreatic DNase added to the reaction mixture. At early times after infection a second replication system, not under control of the gene 43 polymerase, has been detected which synthesizes T4 DNA in toluenized cells.
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PMID:Replication of T4 DNA in Escherichia coli treated with toluene. 458 70

The active forms of 6-(p-hydroxyphenylazo)-uracil and 6-(p-hydroxyphenylazo)-isocytosine were isolated and identified as their respective hydrazino derivatives. These arylhydrazino pyrimidines selectively inhibited a chromatographically distinct DNA polymerase from Bacillus subtilis. The actions of the reduced drugs on this polymerase were identical to those observed on ATP-dependent DNA synthesis in toluene-treated cells; dGTP competitively antagonized the inhibitory activity of the uracil derivative, and dATP competitively antagonized that of the isocytosine derivative. Analysis of the interactions of the arylhydrazinopyrimidines and nucleic acid bases by nuclear magnetic resonance suggested that hydroxyphenylhydrazino-uracil and hydroxyphenylhydrazino-isocytosine pair in a novel manner with, respectively, cytosine and thymine. A mechanism of inhibitor action, involving binding of the reduced drugs to enzyme and the pyrimidines of DNA template, is proposed.
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PMID:Hydroxyphenylazopyrimidines: characterization of the active forms and their inhibitory action on a DNA polymerase from Bacillus subtilis. 463 57


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