The Effect of R Plasmid R391 on UV-sensitivity, Spontaneous and UV-induced Mutagenesis in E̲s̲c̲h̲e̲r̲i̲c̲h̲i̲a̲ C̲o̲l̲i̲ PDF Download
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Author: Marti S. Magarian
Publisher:
ISBN:
Category : DNA repair
Languages : en
Pages : 102
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Author: Marti S. Magarian
Publisher:
ISBN:
Category : DNA repair
Languages : en
Pages : 102
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Author: Doris L. Spanggord
Publisher:
ISBN:
Category : Escherichia coli
Languages : en
Pages : 94
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Author: Neeru Khosla
Publisher:
ISBN:
Category : Escherichia coli
Languages : en
Pages : 94
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Author: Jefferson Woodard
Publisher:
ISBN:
Category : Escherichia coli
Languages : en
Pages : 76
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Author:
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Category :
Languages : en
Pages : 0
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Experiments have shown that induction of mutations to rifampicin-resistance occurs after UV-irradiation in bacteria carrying a deletion through the polA gene, demonstrating that DNA polymerase I (Pol I) is not an essential enzyme in this process. Although it remained an open question whether Pol I is able to participate when it is present. By demonstrating that UV light is unable to induce rifampicin-resistant mutations in a temperature-sensitive E.coli strain lacking a functional DNA polymerase III alpha- subunit, it was concluded that a functional DnaE protein is essential for UV mutagenesis. UV mutability was restored by the presence of a plasmid carrying the dnaE+ allele. Experiments showed that DnaE protein is required for the process of misincorporation opposite a lesion as revealed by delayed photoreversal. A series of genetic experiments were carried out involving immediate and delayed photoreversal which demonstrated that RecA protein plays a third essential role in the process of UV-induced mutagenesis. Either RecA does not require activation for this third role, or activation is occurring as an inevitable consequence of binding at the site of the lesion itself. Thè recA1730 allele was shown to be dominant to recA* and to block the bypass stage of mutagenesis rather than the misincorporation step, indicating that the third role of RecA may be in this second stage. The umuC mutations umuC36 and umuC122::TnlO block UV- induced mutagenesis. umuC36 is a point mutation producing a non-functional UmuC protein, whereas umuC122 is an insertional mutation and no protein is produced. Experiments have shown that, in the absence of excision repair or in the presence of acriflavine, overproduction of either UmuD or UmuD' proteins from a plasmid causes suppression of the umuC36 phenotype but not umuC122. That is, a umuC3 6 mutant in the absence of excision repair is UV-mutable if UmuD or umuD' is overproduced. Preliminary in vitro experiments using DNA sequencing techniques of a UV-irradiated M13 template have implicated that DNA polymerase II has the potential to bypass pyrimidine dimers.
Author: Helen Joy Bates
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Author: Alexander Hollaender
Publisher: Springer
ISBN: 9780306421716
Category : Medical
Languages : en
Pages : 700
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Volume 9 of Chemical Mutagens consists mainly of chapters discussing the development and validation of short-term assays to detect the mutagenic effects of environmental chemicals. These chapters include an assay with the grasshopper neuroblast, a comparison of mutagenic responses of human lung-derived and skin-derived diploid fibroblasts, a forward-mutation assay in Salmonella, a multigene sporulation test in Bacillus subtilis, a specific locus assay in mouse lymphoma cells, a study of the induction of bacteriophage lambda, and the granuloma pouch assay. In addition, there are two chapters on the identification of mutagens in cooked food and in human feces. Frederick 1. de Serres Research Triangle Park, North Carolina vii Contents Chapter 1 The Grasshopper Neuroblast Short-Term Assay for Evaluating the Effects of Environmental Chemicals on Chromosomes and Cell Kinetics 1 Mary Esther Gaulden, Jan C. Liang, and Martha J. Ferguson 1. Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 2. Embryo Supply. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 2. 1. Species. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 2. 2. Origin of Colonies . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 2. 3. Life Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 2. 4. Colony Maintenance . . . . . . . . . . . . . . . . . . . . . . . . . 6 2. 5. Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 2. 6. Allergy to Grasshoppers . . . . . . . . . . . . . . . . . . . . . . 14 3. Grasshopper Egg, Embryo, and Cells . . . . . . . . . . . . . . . . . 14 3. 1. The Egg Shell and Membranes . . . . . . . . . . . . . . . . . 14 3. 2. Embryonic Development . . . . . . . . . . . . . . . . . . . . . . 17 3. 3. Cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 4. Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 4. 1. Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 4. 2. Preparation of Embryos for Cell Analysis . . . . . . . . . 34 4. 3. Analysis of Mutagen Effects. . . . . . . . . . . . . . . . . 40 . . . 5. Response of the Grasshopper Neuroblast to Mutagens . . . . 50 5. 1. Reproducibility of Data . . . . . . . . . . . . . . . . . . . . . . . 50 5. 2. Radiation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 5. 3. Chemical Mutagens . . . . . . . . . . . . . . . . . . . . . . . . . .
Author: Manfred T. Kittel
Publisher:
ISBN:
Category : DNA repair
Languages : en
Pages : 118
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Author: Martinus R. Schaaper
Publisher:
ISBN:
Category :
Languages : en
Pages : 106
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Author: DNA Repair Information Network
Publisher:
ISBN:
Category : Science
Languages : en
Pages : 376
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