Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.7.7.7 (DNA polymerase)
17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of six deoxyribonucleic acid repair mutants of Bacillus subtilis assayed for deoxyribonucleic acid polymerase, only the methyl methanesulfonate-sensitive and ultraviolet light-sensitive mutant JB1-49(59) has impaired polymerase activity. Extracts prepared by sonic treatment or gentle lysis had about 10% of the wild-type activity with poly d(A-T), an alternating copolymer of deoxyadenylate and deoxythymidylate, used as template. The sensitivity to methyl methanesulfonate and ultraviolet light and the low level of polymerase activity transformed and reverted together, indicating that the two characteristics are a pleiotropic manifestation of a single mutation. Mixed extract and kinetic experiments mitigated against an altered nuclease activity as the enzymatic consequence of the mutation. Also, the mutant and wild type activities were stimulated equally by Escherichia coli exonuclease III. The residual activity in the mutant showed several differences from the wild-type activity: it purified differently, was more sensitive to sulfhydryl reagents, and displayed a different template specificity. We tentatively conclude that either the mutation in JB1-49(59) has introduced a qualitative as well as a quantitative change in the polymerase or the wild type contains two distinct polymerases, one of which is missing in the mutant.
...
PMID:Altered deoxyribonucleic acid polymerase activity in a methyl methanesulfonate-sensitive mutant of Bacillus subtilis. 433 Jul 38

Attempts to transduce the ultraviolet-sensitive mutator lesion mutU4 into strains deficient in deoxyribonucleic acid polymerase I (polA) were unsuccessful. Mutator recombinants were found when the polA recipient had first been reverted to Pol(+) by selection for resistance to methyl methanesulfonate. The inviability of the mutU4 polA double mutant was demonstrated by a reduction in the absolute number of transductants when the recipient was polA as compared with Pol(+), and selection was made for markers very close to mutU4. Double mutants containing mutU4 and polA4, which determines a cold-sensitive polymerase, were unable to grow at 24 C, the nonpermissive temperature.
...
PMID:Ultraviolet-sensitive mutator mutU4 of Escherichia coli inviable with polA. 434 45

A mutant strain of E. coli, initially identified by an abnormally high frequency of recombination, has been found to be defective in the 5' --> 3' exonuclease associated with DNA polymerase I, but not in the polymerase activity. This defect is tolerated at 30 degrees , but is lethal at 43 degrees . Like other polymerase I mutants, the strain is unusually sensitive to methyl methanesulfonate and to ultraviolet irradiation; it is also unable to support the growth of phage lambda defective in general recombination, and shows a reduced rate of joining of 10S "Okazaki fragments." These results demonstrate that a functional DNA polymerase I is essential for normal growth and viability in E. coli K12.
...
PMID:A conditional lethal mutant of Escherichia coli K12 defective in the 5' leads to 3' exonuclease associated with DNA polymerase I. 460 Jul 86

A series of mutations of Bacillus subtilis, conferring sensitivity to methyl methanesulfonate (MMS), were transferred by transformation to a suppressible his(-) stock. The introduction of certain sensitivity mutations prevented the ultraviolet- or MMS-induced, but not the spontaneous, reversion of his(-) to his(+). Not all sensitivity mutations led to this resistance to mutagenesis; a strain with altered deoxyribonucleic acid (DNA) polymerase activity behaved almost normally with respect to its mutagen response, as did an excision-defective, ultraviolet-sensitive strain used as a control. One of the mutagen-stable strains responded to mutagenesis with nitrosomethylguanidine; another appeared stable even to this mutagen. All mutagen-stable strains had DNA polymerase and DNA ligase activity.
...
PMID:Mutagen stability of alkylation-sensitive mutants of Bacillus subtilis. 462 5

Many temperature-resistant revertants of a polA1 polB polCts (HS432) strain are PolI+ (by either suppression of the polA1 amber allele or intragenic reversion) but remain polCts (contain a temperature-sensitive DNA polymerase III). It appears that DNA replication in such temperature-resistant revertants depends on an extragenic mutation, pcbA, already present in the parent strain and not linked to any of the DNA polymerase loci. This allele allows DNA replication dependent on DNA polymerase I and bypasses a temperature-sensitive DNA polymerase III (polC bypass), so that reversion to PolI+ makes the strain temperature resistant. This pathway of DNA replication also supports phage and plasmid DNA replication. At restrictive temperature, these mutants display a normal response to UV irradiation but show increased sensitivity to the alkylating agent methyl methanesulfonate. We have located pcbA linked to dnaA.
...
PMID:Map location of the pcbA mutation and physiology of the mutant. 632 87

Seven different test systems were utilized to investigate the genetic activity of chromium compounds: infidelity of DNA replication in vitro by DNA pol alpha from calf thymus, damage of DNA detected by alkaline elution in treated mammalian cells or in DNA purified and treated in vitro, DNA repair synthesis in mammalian cells in vitro detected by autoradiography or scintillation counting after labelling with [3H]dThd, gene mutations in the Salmonella typhimurium Ames test, gene mutations (6TG resistance) in cultured hamster cells, sister-chromatid exchanges in different rodent cell cultures, and transformation to anchorage-independent growth of hamster cells in vitro (soft-agar assay). Potassium dichromate and chromium chloride were used as water-soluble Cr(VI) and Cr(III) salts. Several reference mutagens (EMS, MMS, MMC, 4NQO) were included in the single tests as positive controls. Cr(VI) was active in all the tested systems, except in the induction of DNA damage and DNA repair synthesis in cultured cells. Cr(III), on the other hand, was absolutely inactive unless a direct interaction with purified DNA was permitted by the test conditions. The relevance of data from the various tests to the understanding of the mechanisms of the genotoxic activity of chromium is discussed. Effects other than the direct interaction of Cr(III) with DNA are inferred, which can cause infidelity of the DNA polymerase functions.
...
PMID:Genetic effects of chromium compounds. 634 55

The synthetic DNA polymers, poly(dG-dC), poly(dC), poly(dA-dT), poly(dA) and poly(dT), were treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methyl methanesulfonate (MMS) and UV irradiation. The modified polymers were used as templates to examine the incorporation of non-complementary nucleotides by E. coli DNA polymerase I. Methylation of poly(dG-dC) by MNNG predominantly induced the misincorporation of dTMP, whereas methylation by MMS induced that of dAMP. Treatment of poly(dT) with MNNG caused the misincorporation of dGMP to a considerable extent, but MMS did not enhance the error on poly(dT). The misincorporation of dAMP on poly(dC) and that of dGMP on poly(dA) were also increased by these chemicals. UV irradiation of poly(dT) and poly(dC) induced the error of dGMP and dAMP, respectively. These data on MNNG and MMS in vitro were in fair agreement with the directions of mutation in vivo. But the predominant induction of transitions by UV in vitro did not agree with the UV-induced transversions in E. coli. This inconsistency suggested the participation of other factors than direct mispairing in UV-induced transversion. Modification of DNA polymerase I by MNNG changed the ratio of polymerase to 3' leads to 5' exonuclease activity altering the fidelity of this enzyme, whereas MMS and UV-irradiation did not alter the fidelity of the enzyme.
...
PMID:Misincorporation in DNA synthesis after modification of template or polymerase by MNNG, MMS and UV radiation. 634 75

During the development of competency in Bacillus subtilis there was an increased sensitivity to methyl methanesulfonate (MMS) treatments. The frequency of reverse mutation also increased among the MMS-revertible markers by a factor of 100 as compared to vegetative cultures. The frequency of 2-aminopurine(AP)-induced mutagenesis was the same in competent and noncompetent cultures. Studies with DNA-polymerase-deficient mutants showed a direct involvement of DNA polymerase I in promoting MMS and transformation-induced mutagenesis in competent cells.
...
PMID:Mutagenesis during transformation of Bacillus subtilis. II. An increase in chemically-induced mutations during competency. 679 10

Mutants of Shigella sonnei (S. sonnei) deficient in DNA polymerase I were isolated after mutagenesis with nitrosoguanidine. The isolation of the mutants was facilitated by the use of a strain harboring plasmid pBR313 which required DNA polymerase I for its muliplication. The mutants isolated could not maintain the plasmid and became sensitive to methyl methanesulfonate (MMS) and to ultraviolet light (UV) irradiation. Assays performed on crude extracts established that the mutants were deficient in an enzyme with DNA polymerase activity. All of these properties are the same as those of E. coli polA. Several MMS-resistant revertants isolated from one of the S. sonnei polA mutants regained 3-120% of the DNA polymerase activity found in the extracts of the wild-type parent strain. Most though not all of the revertants could support the multiplication of plasmid pBR313.
...
PMID:Mutants of Shigella sonnei deficient in DNA polymerase I. 702 49

Alkylatio of Escherichia coli DNA that have been made permeable to nucleotides by toluene treatment results in the expression of DNA polymerase I-directed repair synthesis. The system only permits measurement of DNA polymerase I-directed repair synthesis. The latter is not observed in mutant cells deficient in this polymerase. DNA ligation is intentionally prevented by the addition of the inhibitor, nicotinamide mononucleotide. MNU, ENU and MMS elicit DNA polymerase I-directed repair synthesis. MNU and MMS are especially potent in this regard, while EMS is a poor inducer of DNA polymerase I activity in permeabilized cells. The natural compound para-aminobenzoic acid itself (0,0002 mM - 20 mM) doesn't induce DNA polymerase I-directed repair synthesis. However, when PABA is used in complex with alkylating agents as the inducers, the repair synthesis increased 2,0, 1,2 and 2,8 times for MNU, ENU and EMS, respectively, as compared to that elicited by "pure" mutagens. The increasing of DNA repair synthesis in permeabilized bacteria in the experiments with PABA may serve as the foundation for its reparagenic activity. The latter was discovered previously by the authors in experiments on mutagenesis of bacterial cells.
...
PMID:[Genetic activity of para-aminobenzoic acid. The intensification of DNA polymerase I-dependent repair induced by chemical mutagens in toluene-treated Escherichia coli cells]. 704 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---