Induced Mutagenesis in Escherichia Coli PDF Download
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Author: Martinus R. Schaaper
Publisher:
ISBN:
Category :
Languages : en
Pages : 106
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Author: Martinus R. Schaaper
Publisher:
ISBN:
Category :
Languages : en
Pages : 106
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Author: Helen Joy Bates
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Category :
Languages : en
Pages :
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Author:
Publisher:
ISBN:
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: Guy Tomer
Publisher:
ISBN:
Category :
Languages : en
Pages : 117
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Author: Manfred T. Kittel
Publisher:
ISBN:
Category : DNA repair
Languages : en
Pages : 118
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Author: Jefferson Woodard
Publisher:
ISBN:
Category : Escherichia coli
Languages : en
Pages : 76
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Author: Zhehong Cai
Publisher:
ISBN:
Category :
Languages : en
Pages : 218
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Author: Angela Mary Keogh
Publisher:
ISBN:
Category :
Languages : en
Pages : 558
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Author: David Mittelman
Publisher: Springer Science & Business Media
ISBN: 1461462800
Category : Medical
Languages : en
Pages : 284
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The discovery of stress-induced mutagenesis has changed ideas about mutation and evolution, and revealed mutagenic programs that differ from standard spontaneous mutagenesis in rapidly proliferating cells. The stress-induced mutations occur during growth-limiting stress, and can include adaptive mutations that allow growth in the otherwise growth-limiting environment. The stress responses increase mutagenesis specifically when cells are maladapted to their environments, i.e. are stressed, potentially accelerating evolution then. The mutation mechanism also includes temporary suspension of post-synthesis mismatch repair, resembling mutagenesis characteristic of some cancers. Stress-induced mutation mechanisms may provide important models for genome instability underlying some cancers and genetic diseases, resistance to chemotherapeutic and antibiotic drugs, pathogenicity of microbes, and many other important evolutionary processes. This book covers pathways of stress-induced mutagenesis in all systems. The principle focus is mammalian systems, but much of what is known of these pathways comes from non-mammalian systems.
Author: Christopher W. Lawrence
Publisher: Springer Science & Business Media
ISBN: 1468443828
Category : Medical
Languages : en
Pages : 433
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Concern is often expressed that our environment may include an increasingly large variety of mutagens, but the extent of the potential hazard they pose has yet to be fully evaluated. A variety of empirical procedures has been devised with which to estimate the mutagenic potency of suspect agents, and the relative merits of different tests are currently under debate. Although such tests are of great value, and are indeed indispensable, they are not, nevertheless, sufficient. In the long term, accurate estimation of hazard will also require a better understanding of the various mechanisms of mutagenesis, and in many instances these remain remarkably elusive. Our knowledge and appreciation of the problem has increased substantially over the last few years, but the precise way in which many mutagens cause mutations is not yet known. The aims of this conference were therefore two-fold. The first was to survey present information about mutagenic mechanisms, drawing together data from work with various experimental approaches and organisms, in order to discern the principles governing the action of different mutagens. The second was to examine the implications of such principles for the execution and evaluation of test procedures, and critically assess the research areas that need further attention in order to improve the interpretation of test results. Chris Lawrence v ACKNOWLEDGEMENT We gratefully acknowledge the support provided for this Conference by the U.,S. Department of Energy, The Foundation for Microbiology, Exxon Corporation and the University of Rochester.
