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)

High molecular weight RNA (35S) isolated from avian myeloblastosis virus directs the cell-free synthesis of two prominent polypeptides of 180,000 and 76,000 molecular weight. The latter polypeptide has previously been identified as the precursor to the group-specific antigens of the virus ("gag" proteins) [Vogt, V. M., Eisenman, R. & Diggelmann, H. (1975) J. Mol. Biol. 96, 471-493]. Two-dimensional tryptic peptide analyses of the [35S]methionine-labeled peptides demonstrate that the 180,000-dalton product is a polyprotein that can account for all the peptides of the avian myeloblastosis virus DNA polymerase (DNA nucleotidyltransferase, EC 2.7.7.7) and those of the gag viral proteins. This is direct confirmation of the genomic order of the viral structural genes, placing the polymerase gene adjacent to the 5'-proximal gag gene of the virus. Furthermore, our findings suggest that the primary polymerase gene product is the beta subunit of the enzyme. These results are discussed in relation to the proposed structural gene map for the avian retraviruses and suggest a model for the in vivo processing of the viral polymerase.
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PMID:Cell-free synthesis of the precursor polypeptide for avian myeloblastosis virus DNA polymerase. 20 Sep 40

The replication of the ColEl plasmid was studied in extracts from E. coli dnaG mutants. It was found that the synthesis of the complementary strands of ColEl DNA can be carried out in these extracts in two consecutive steps: (1) synthesis of the leading L strand independent of the dnaG function, and (2) synthesis of the lagging H strand depending upon addition of wild-type dnaG protein. In contrast to L strand synthesis, the latter reaction is insensitive to rifampicin and novobiocin. Both synthetic pathways are however blocked by antiserum directed against dnaB protein. This indicates an additional role of the dnaB protein in duplex DNA replication besides assisting the dnaG protein in the priming of lagging strand synthesis. The T7 gene-4 protein acting in conjunction with T7 DNA polymerase can substitute for both the function of the dnaB and dnaG protein. It is concluded that plasmid replication proceeds by a semi-discontinuous mechanism.
Mol Gen Genet 1979
PMID:Replication of the colicin E1 plasmid in extracts of Escherichia coli: uncoupling of leading strand from lagging strand synthesis. 23 24

A new method for determining nucleotide sequences in DNA is described. It is similar to the "plus and minus" method [Sanger, F. & Coulson, A. R. (1975) J. Mol. Biol. 94, 441-448] but makes use of the 2',3'-dideoxy and arabinonucleoside analogues of the normal deoxynucleoside triphosphates, which act as specific chain-terminating inhibitors of DNA polymerase. The technique has been applied to the DNA of bacteriophage varphiX174 and is more rapid and more accurate than either the plus or the minus method.
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PMID:DNA sequencing with chain-terminating inhibitors. 27 68

Cleavage sites on the pWWO-8 plasmid were determined for the restriction endonucleases HindIII and XhoI. Terminal labelling using DNA polymerase I was particularly useful both for the characterisation of the smaller cleavage products and for confirmation of the order of fragments in the intact plasmid.
Mol Gen Genet 1979 Jan 05
PMID:An endonuclease cleavage map of the plasmid pWWO-8, a derivative of the TOL plasmid of Pseudomonas putida mt-2. 28 16

The effect of phage T4 gene 43 (DNA polymerase) mutations on recombination between adjacent base pairs was measured in rII amber and opal mutants. The mutator allele tsL56 did not promote recombination frequencies at the two sites in which its effect was studied. The antimutator allele tsCB87 caused slight or no reduction in recombination frequencies at five sites.
Mol Gen Genet 1979 Jan 11
PMID:Recombination in phage T4 gene-43 (DNA polymerase) mutants. 28 43

The ultraviolet (UV) sensitivity of Escherichia coli mutants deficient in the 5' leads to 3' exonuclease activity of DNA polymerase I is intermediate between that of pol+ strains and mutants which are deficient in the polymerizing activity of pol I (polA1). Like polA1 mutants, the 5'-exonclease deficient mutants exhibit increased UV-induced DNA degradation and increased repair synthesis compared to a pol+ strain, although the increase is not as great as in polA1 or in the conditionally lethal mutant BT4113ts deficient in both polymerase I activities. When dimer excision was measured at UV doses low enough to avoid interference from extensive DNA degradation, all three classes of polymerase I deficient mutants were found to remove dimers efficiently from their DNA. We conclude that enzymes alternative to polymerase I can operate in both the excision and resynthesis steps of excision repair and that substitution for either of the polymerase I functions results in longer patches of repair. A model is proposed detailing the possible events in the alternative pathways.
Mol Gen Genet 1977 Jan 07
PMID:Excision-repair in mutants of Escherichia coli deficient in DNA polymerase I and/or its associated 5' leads to 3' exonuclease. 31 38

The induction of prophage lambda by ultraviolet light has been measured in E. coli K12 lysogenic cells deficient in DNA polymerase I. The efficiency of the induction process was greater in polA1 polC(dnaE) double mutants incubated at the temperature that blocks DNA replication than in polA+ polC single mutants. Similarly, the polA1 mutation sensitized tif-promoted lysogenic induction in a polA1 tif strain at 42 degrees. In strains bearing the polA12 mutation, which growth normally at 30 degrees, induction of the prophage occurred after the shift to 42 degrees. It is concluded that dissapearance of the DNA polymerase I activity leads to changes in DNA replication that are able, per se, trigger the prophage induction process.
Mol Gen Genet 1977 Sep 09
PMID:Prophage induction in Escherichia coli K12 cells deficient in DNA polymerase I. 33 8

The mutation recL152 leads to a reduction of excision repair as measured by an increase in the time required to close uvrA uvrB dependent incision breaks, and by a reduction of host cell reactivation ability. Postreplication repair is also delayed when measured in a uvrB5 recL152 double mutant. Such a determination could not be made using the recL152 single mutant because the excision defect led to an accumulation of breaks in the unlabeled high molecular weight DNA to which the labeled DNA synthesized after irradiation must attach in order to achieve normal high molecular weight. Further, the recL gene product seems to be required to rejoin breaks in parental strand DNA which are generated during postreplication repair, since such gaps accumulate in a recL152 uvrB5 double mutant but not in a recL+ uvrB5 single mutant. We have noticed a striking phenotypic similarity between recL152 and polA1 and suggest that recL152 is required for full in vivo activity of DNA polymerase I.
Mol Gen Genet 1977 Oct 24
PMID:Defective excision and postreplication repair of UV-damaged DNA in a recL mutant strain of E. coli K-12. 34 Aug 83

The replication cycle of the small resistance plasmid RSF1030 can be divided into two stages with different enzyme requirements: (1) Synthesis of early replicative intermediates containing 7 S DNA catalyzed by DNA polymerase I in the absence of functional dnaZ protein, and (2) replication of early intermediates requiring DNA polymerase III holenzyme (including the dnaZ protein). Early intermediate DNA synthesized in a dnaZ extract can be converted to fully replicated plasmid molecules upon addition to a replication enzyme fraction prepared by ammonium sulfate fractionation of polA I extracts. The first-stage reaction is sensitive to rifampicin, novobiocin, and oxolinic acid, but insensitive to arabinosylcytosine triphosphate (aCTP). Addition of aCTP interferes with the second-stage reaction resulting in the accumulation of late replicative intermediates.
Mol Gen Genet 1977 Nov 04
PMID:Replication of the ampicillin resistance plasmid RSF1030 in extracts of Escherichia coli: separation of the replication cycle into early and late stages. 34 Aug 89

Toluene treated cells have been used to study the processes of DNA synthesis and DNA degradation in ultra-violet irradiated Escherichia coli K12. Synthesis and degradation are both shown to occur extensively if polynucleotide ligase is inhibited, and to occur to a much lesser extent if ligase activity is optimal. Extensive UV-induced DNA synthesis in toluene-treated cells requires ATP for the initial incision step, and DNA polymerase I. Extensive degradation also depends on the early ATP-dependent incision step, and the subsequent degradation shows a partial requirement for ATP. Curtailment of degradation by ligase requires DNA polymerase activity, but is not dependent upon DNA polymerase I. Apparently this process can be carried out with equal facility by either DNA polymerase II or polymerase III. These observations suggest that extensive DNA polymerase I-dependent repair synthesis and extensive DNA degradation are facets of two divergent pathways of excision repair, both of which depend upon the early uvrABC determined ATP-dependent incision step.
Mol Gen Genet 1977 Nov 29
PMID:DNA synthesis and degradation in UV-irradiated toluene treated cells of E. coli K12: the role of polynucleotide ligase. 34 Sep 17


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