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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)

A deficiency in DNA polymerase I increased the ultraviolet (UV) radiation sensitivity of a uvrA strain of Escherichia coli K-12 when plated on minimal growth medium. The slope of the survival curve for the uvrA polA strain was 2.0-times greater than that for the uvrA strain. The fluence-dependent yield of unrepaired deoxyribonucleic acid (DNA) parental-strand breaks following UV irradiation and incubation in minimal growth medium was similar in both strains. However, the fluence-dependent yield of unrepaired DNA daughter-strand gaps observed following UV irradiation was 1.8-fold greater in the uvrA polA strain than in the uvrA strain. These results suggest that DNA polymerase I is involved in the filling of at least some daughter-strand gaps during postreplication repair. Also, the uvrA polA strain was sensitized by a post-UV treatment with chloramphenicol (CAP) to a similar extent as was the uvrA strain, indicating that DNA polymerase I is not involved in the CAP-inhibitable pathway of postreplication repair.
Mol Gen Genet 1978 Nov 16
PMID:The involvement of DNA polymerase I in the postreplication repair of ultraviolet radiation-induced damage in Escherichia coli K-12. 36 86

Escherichia coli mutants defective in DNA uracil N-glycosidase (ung-) or endonuclease VI active against apurinic/apyrimidinic sites in DNA (xthA-) exhibit enhanced sensitivity towards 5-bromodeoxyuridine relative to the wild type strain, pointing to involvement of these enzymes in repair of bromouracil-induced lesions in DNA. Mutants defective in DNA polymerase I, either in polymerizing activity (polAl-) or (5' leads to 3')-exonuclease activity (polA107-) exhibit unusually high sensitivity (including marked lethality) in the presence of 5-bromodeoxyuridine. The results indicate that DNA polymerase I, and its associated (5'--3')-exonuclease activity, are involved in repair of bromouracil-induced lesions and are not readily replaced, if at all, by DNA polymerases II and III. Thermosensitive mutant in DNA ligase gene (lig ts7) shows high sensitivity towards 5-bromodeoxyuridine at 42 degrees C indicating the role of the enzyme in repair of bromouracil-induced lesions in DNA. Involvement of DNA uracil N-glycosidase, and endonuclease active against apurinic/apyrimidinic sites in recognition and repair of 5-bromouracil-induced damage permits of some inferences regarding the nature of this damage (lesions), in particular dehalogenation of incorporated bromouracil to uracil residues.
Mol Gen Genet 1979 Mar 20
PMID:Genetic evidence for the nature, and excision repair, of DNA lesions resulting from incorporation of 5-bromouracil. 37 26

Using phiX1974 replicative form (RF) DNA as an in vivo probe, we have investigated the coordinated action of the 5' leads to 3' exonuclease and polymerase activities of DNA polymerase I in order to understand better its physiological role. We constructed double mutants containing the rep mutation (the replication of phiX174 RF does not occur in rep mutants) together with a mutation affecting DNA polymerase I, either polA12 or polA546ex. Using these mutants, which are believed to be thermosensitive in the polymerase function or the 5' leads to 3' exonuclease function respectively, we studied the kinetics of nick translation at the permissive and non-permissive temperatures in vivo. The substrate was the phiX174 replicative form DNA nicked by the phiX174 gene A protein. E. coli rep polA546ex gave the lowest rate of nick translation, although the ability to perform nick translation, at least as measured by our assay, was still present. E. coli rep polA12 showed a similar low rate at the non-permissive temperature but a rate close to the wild-type level at the permissive temperature. Formation of the parental replicative form molecule in either strain was affected little, even at the restrictive temperature. Our results suggest that DNA polymerase I may not play a major role in ongoing DNA replication.
Mol Gen Genet 1979 Apr 17
PMID:"Nick translation" in Escherichia coli rep strains deficient in DNA polymerase I activities. 37 26

Vaccinia virus DNA polymerase will utilize a substrate consisting of phi X174 DNA primed with a strand of a unique restriction fragment, but the reaction is inefficient. Examination of the reaction products by alkaline agarose gel electrophoresis revealed a few discrete fragments, each corresponding to an extended primer strand. This result implies that specific barriers exist on the phi X174 template which impede, but do not completely halt, the progress of the enzyme. Only a few per cent of the template molecules were completely copied. Similar findings were reported by Sherman and Gefter using Escherichia coli DNA polymerase II and fd DNA (J. Mol. Biol. (1976) 103, 61-76). Several observations suggest that the barriers are regions of template secondary structure. Some barriers are more effective than others, and they increase in both effectiveness and number as the temperature is decreased. The same barriers are observed with T4 DNA polymerase, but none are detected with E. coli DNA polymerase I. Finally, the major barriers are located in regions of the phi X174 sequence known to contain hairpin structures of relatively high stability. The exact stopping point of one of the major barriers is within the duplex stem of a hairpin structure. These results show that DNA polymerases are a useful probe of the secondary structure of a single-stranded DNA.
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PMID:The effect of template secondary structure on vaccinia DNA polymerase. 38 Dec 93

The interaction of pyridoxal, pyridoxal-5'-mono-, di- and triphosphate with certain enzymes of polynucleotide synthesis (DNA-dependent RNA polymerase, DNA-dependent DNA polymerase I and polynucleotide phosphorylase from Escherichia coli and terminal deoxyribonucleotide transferase from calf thymus) was studied. All compounds tested was found to be reversible and competitive inhibitors of these enzymes. The reduction of the enzyme-inhibitor complex with NaBH4 gives rise to the complete irreversible inhibition of the enzymes under study. The comparison of the inhibition constants for pyridoxal and its phosphorylated derivatives with those for mono-, di- and triphosphates of nucleosides was carried out for the enzymes. The results obtained suggest that the modified epsilon-amino-group of lysine residue should be localized at the catalytic site in the vicinity of the pyrophosphate binding area of an enzyme.
Mol Biol (Mosk)
PMID:[Interaction of oligophosphates of pyridoxal with certain enzymes of polynucleotide synthesis]. 38 98

The number of pyrimidine dimers (sites sensitive to UV-endonuclease from M. luteus) transferred at 43 degrees to daughter DNA strands during postreplication repair in UV-irradiated E. coli uvr A polCts was found to be decreased as compared to that after repair at 32 degrees. This indicates the involvement of DNA polymerase III in the sister DNA recombination in UV-irradiated E. coli.
Mol Gen Genet 1979 Jun 20
PMID:Decreased transfer of pyrimidine dimers from parental to daughter DNA strands in UV-irradiated Escherichia coli deficient in DNA polymerase III. 38 55

The relationship between replication control and plasmid incompatibility has been investigated using a composite replicon, pPM1, which consists of the pSC101 plasmid ligated to another small multicopy plasmid, RSF1050. Since pPM1 can utilise the replication system of either of the two functionally distinct components, propagation of the composite plasmid can occur in the presence of a mutation of one of its moieties. Such mutants are detected by their inability to rescue the composite plasmid under conditions not permissive for replication of the other moiety. Mutations in incompatibility functions can be detected by the failure of the composite replicon to exclude co-existing plasmids carrying a replication system identical to the one on pPM1. The inability of the composite plasmid to replicate at 42 degrees in a host synthesizing temperature-sensitive DNA polymerase I, which is required by the RSF1050 replication system, was used to isolate pPM1 mutants defective in replication of the pSC101 component. Mutants defective in the incompatibility functions of pSC101 were obtained by selecting derivatives that allow the stable coexistence of a second pSC101 replicon in the same cell. Analysis of these two classes of mutants indicates that plasmids selected for defective pSC101 replication ability nervertheless retain pSC101 incompatibility. In contrast, plasmid mutants that have lost incompatibility functions were found always to be defective in replication ability.
Mol Gen Genet 1979 Jul 13
PMID:Genetic analysis of the inter-relationship between plasmid replication and incompatibility. 38 41

Synthesis of DNA complementary to the transferred strand of an IncI alpha plasmid has been shown previously to require DNA polymerase III. The possible involvement of the two defined priming proteins of Escherichia coli K12, RNA polymerase and primase, in initiating this conjugal DNA synthesis had been examined. Primase was inactivated using temperature-sensitive dnaG3 mutants and RNA polymerase was inhibited using rifampicin. When these two proteins were simultaneously inactivated in both parental strains, the average recipient synthesised at least one single-stranded equivalent of R144drd-3 before the rifampicin-treated donors lost the ability to transmit DNA. It is proposed that the product of a plasmid transfer gene is responsible for initiating this DNA synthesis in recipients. The results imply that this protein is supplied by the donors.
Mol Gen Genet 1979 Oct 01
PMID:A novel priming system for conjugal synthesis of an IncI alpha plasmid in recipients. 39 29

Following UV irradiation of Bacillus subtilis there is a coordinate induction of: 1) a new protein, 2) a W-reactivation system, 3) a DNA modification system, and 4) prophages. These functions are induced following UV irradiation of repair proficient bacteria and mutants deficient in excision repair (UVR-1) and DNA polymerase I activity (polA5). However, they are not induced, or are impaired in their ability to be induced in bacteria containing the recA1 and the recG13 mutations. This inducible system is compared to the SOS system observed in E. coli.
Mol Gen Genet 1977 Jun 08
PMID:DNA repair in Bacillus subtilis. I. The presence of an inducible system. 40 45

Transversion mutations can be distinguished from transition mutations by the use of special tauII mutants of bacteriophage T4. Methyl methanesulfonate did not induce reversion of the tester mutants along transversion or transition pathways from A:T1 base pair sites, nor along transversion pathways from G:C base pair sites. Ethyl methanesulfonate and N-methyl-N-nitrosourea, however, induced both transversions and transitions at an A:T base pair site; no transversions were detected at G:C-sites. Mn++ induced transversions and transitions at both A:T-and G:C-sites. The influence of temperature-sensitive gene-43 DNA polymerase mutator and antimutator mutations on the reversion of the tauII tester mutants was measured: some gene-43 mutants differentially influenced different pathways of reversion. Studies of thymineless mutagenesis demonstrated A:T-site transversion mutations. A synergistic interaction between thymineless mutagenesis and the gene-43 mutator, tsL56, was used to demonstrate thymineless mutagenesis at one site where it was not detected in the presence of the wild type polymerase.
Mol Gen Genet 1975 Nov 03
PMID:Transversion mutagenesis in bacteriophage T4. 76 23


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