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)

Discontinuities of T4 DNA which are caused by excision of UV-damaged areas, by decay of (32)P atoms, or which are present in DNA from rII(-)lig(am) (-) phage produced in a host nonpermissive for amber mutants are all repaired by bacterial enzymes after infection in the presence of chloramphenicol. Escherichia coli DNA polymerase I participates in the host-mediated repair, but an approximately 20-fold variation in the levels of host polynucleotide ligase does not affect either the kinetics or the extent of repair observed. Upon removal of chloramphenicol, host-repaired DNA from UV-irradiated phage undergoes a secondary cycle of breakage, which ultimately results in solubilization of most of the phage DNA. If the cells are co-infected with nonirradiated helper phage, the secondary breaks are repaired and the continuity of the polynucleotide chain is restored. The close coincidence in the extent of primary and secondary breakage suggests that phage-coded enzymes recognize and excise areas improperly repaired by the host. In contrast to host-mediated repair, repair mediated by rescuing phage probably restored functionality to the damaged DNA.
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PMID:Host-mediated repair of discontinuities in DNA from T4 bacteriophage. 458 87

Linear phiX174 single-stranded DNA can be isolated from phiX phage particles produced under various conditions. About half of the linear strands have a dGMP residue at the 5' end, the remaining have roughly comparable amounts of dCMP, dTMP, and dAMP. The linear strands can be converted to covalently closed circular molecules by polynucleotide ligase, but only after they have been incubated with T4 DNA polymerase and deoxynucleoside triphosphates. Experiments with endonuclease R, the restriction enzyme from Haemophilus influenzae, indicated that the nucleotides incorporated into the DNA during this reaction were found predominantly in a limited region of the genome. The results suggest that the normal intermediate in single-stranded phiX174 DNA synthesis may be a single-stranded linear molecule which is shorter than unit length and is intrinsically capable of circularization.
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PMID:Mechanism of replication of single-stranded PhiX174 DNA. VII. Circularization of the progeny viral strand. 459 Oct 49

A DNA-membrane complex isolated from Escherichia coli infected with bacteriophage T7 contains newly synthesized T7 DNA and the T7 DNA polymerase (gene 5 product). The DNA present in the complex appears to exist as a concatemer which contains single-strand breaks and possibly internal single-stranded regions (gaps). The complex is capable of synthesizing T7 DNA by using endogenous template, and part of the DNA is made by a semiconservative mechanism. A portion of the in vitro synthesized DNA sediments in alkaline sucrose as 10-11S material. This DNA is converted to a larger-molecular-weight material after treatment with T4 polynucleotide ligase and E. coli DNA polymerase I.
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PMID:Bacteriophage T7 DNA synthesis in isolated DNA-membrane complexes. 459 Oct 51

Daughter-strand gaps in deoxyribonucleic acid (DNA) synthesized after exposure of excision-deficient Escherichia coli to ultraviolet light are filled during subsequent incubation in buffer, and the rate of filling is increased when the incubation in buffer is carried out in the presence of 360-nm light. It is concluded that daughter-strand discontinuities are prevented from being rapidly sealed in the dark not because of some structural feature of the daughter-strand but because of the presence of a pyrimidine dimer on the opposite (parental) strand. "Photoreactivation-stimulated gap filling" is dependent on the polA(+) and recA(+) but not the exrA(+) genes. It is suggested that the removal of the dimer allows gap-filling by DNA polymerase I and polynucleotide ligase. The recA(+) gene may be needed at a very early stage, possibly for gap stabilization.
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PMID:Effect of photoreactivation on the filling of gaps in deoxyribonucleic acid synthesized after exposure of Escherichia coli to ultraviolet light. 459 42

Bacteriophage T4 has a third pathway for repair of damaged DNA besides excision repair and recombination repair. This pathway is a mechanism for the toleration of lesions rather than the repair of lesions. The substrate for this process is gapped DNA copied from a damaged template. Evidence indicates that these gaps are filled, giving rise to daughter strands that are sensitive to heat and to treatments with RNAase. These daughter strands subsequently serve as templates for DNA that is resistant to RNAase. This third pathway is dependent upon gene 41 (RNA-priming protein), gene uvsZ (function unknown) and gene 30 (polynucleotide ligase) and is presumed to consist of 4 steps: (1) induction of primer RNA opposite the lesion in the template; (2) elongation of primers by DNA polymerase; (3) ligation of daughter-strand fragments, without removal of primer RNA; (4) replication of DNA carrying RNA sequences, giving homogeneous DNA strands. We have called this process 'Re-initiation repair'.
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PMID:Bypass of pyrimidine dimers in DNA of bacteriophage T4 via induction of primer RNA. 618 40

The early steps of excision repair of cyclobutane pyrimidine dimers are investigated. It is demonstrated that the apurinic/apyrimidinic endonuclease associated with the Micrococcus luteus uv-specific endonuclease cleaves the phosphodiester bond on the 3' side of the deoxyribose leaving a 3' hydroxy terminus and a 5' phosphoryl terminus. This nick is not a substrate for T4 polynucleotide ligase. The 3' base-free deoxyribose terminus is not a substrate for either the polymerase or the 3' to 5' exonuclease activities of Escherichia coli DNA polymerase I. However, the 3' terminus of the nick is converted to a substrate for DNA polymerization by the action of a 5' apurinic/apyrimidinic endonuclease. A three-step model for the incision step of excision repair of cyclobutane pyrimidine dimers is presented.
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PMID:Early steps of excision repair of cyclobutane pyrimidine dimers by the Micrococcus luteus endonuclease. A three-step incision model. 626 31

DNA repair proficiency in cells is expressed by various enzymes which can recognize damaged sites arising from exogenous agents or endogenous conditions. Either a damaged base is recognized by DNA glycosylases, partially removed by hemi-DNA glycosylases acting on diadduct damage, or direct incision of the phosphodiester bond near the damaged site. Incision at those apurinic or apyrimidinic sites arising from depurination-depyrimidination or glycosylase reactions is effected by apurinic or apyrimidinic endonucleases. Excision of damaged sites is catalyzed by unique exonucleases followed by DNA polymerase catalyzed reinsertion of nucleotides. The integrity of the strands is restored by polynucleotide ligase when a juxtaposed nucleotide is properly reinserted.
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PMID:Enzymatic mechanisms of DNA repair. 628 49

A cell-free extract from blue-green alga Anacystis nidulans contains enzymes which repair in vitro the transforming activity of gamma-irradiated Bacillus subtilis DNA. The level of restoration of the transforming activity depends on the protein concentration in the reaction mixture, the duration of incubation and on the dose of irradiation. The repair of gamma-induced lesions is most efficient in the presence of magnesium ions, NAD and ATP. The present data indicate that the repair of transforming DNA is performed with the participation of DNA polymerase and polynucleotide ligase which function in the cell-free extract of algae.
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PMID:[In vitro repair of gamma-irradiated transforming Bacillus subtilis DNA by extracts of blue-green algae]. 680 46

We have isolated recombination deficient mutants of Bacillus subtilis on the basis of their sensitivity to methyl-methane-sulfonate or ultraviolet light, or of their inability to be transformed on solid medium. We have analyzed the mutants for several recombination and repair properties; we have grouped them in 5 classes on the basis of their phenotype and tested them for the activity of several enzymes acting on DNA, ie. DNA polymerase, polynucleotide ligase, ATP dependent DNase, and a DNase acting on single-stranded DNA. One mutant was found reduced in the latter DNase. Some of the mutants have been mapped, and they correspond to three different genes denominated rec D, rec F and rec G. All the recombination deficient mutants of B. subtilis described in the literature have been grouped in 7 classes; the mutations belong to 13 (and possibly 15) different genes distributed along the map. A coherent nomenclature and the criteria for a standard study of the rec mutants are proposed.
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PMID:Genetic and enzymic studies on the recombination process in Bacillus subtilis. 1609 63


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