Plasmid-mediated DNA Repair and Mutagenesis in "Escherichia Coli". PDF Download
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Author:
Publisher:
ISBN:
Category : Microbiology (Board of Studies)
Languages : en
Pages : 438
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Book Description
Author:
Publisher:
ISBN:
Category : Microbiology (Board of Studies)
Languages : en
Pages : 438
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Book Description
Author: Noel James Doyle
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Author: Andrei Kuzminov
Publisher: Landes Bioscience
ISBN:
Category : Medical
Languages : en
Pages : 234
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Author: Bradley Theodore Smith
Publisher:
ISBN:
Category : Press
Languages : en
Pages : 316
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Book Description
All organisms face constant challenges to the integrity of their genomes, from environmental agents such as ultraviolet light (UV) to errors generated by their own DNA polymerases. To deal with these challenges, all organisms possess a range of DNA repair and damage tolerance systems. In bacteria, there exists an inducible response to DNA damage termed the SOS response, in which damage induces the expression of greater than forty genes involved in repair. Mismatch repair (MMR) is a system by which the cell is able to avoid mutations by correcting DNA replication errors. Working with living Bacillus subtilis cells, the studies described here have found that MutS and MutL, the key proteins of MMR, form discrete foci in response to mismatches. These MMR foci are the active sites of repair, and appear to assemble near the DNA polymerase at mismatched base-pairs. This is consistent with a model in which the newly-synthesized DNA strand containing the error is discriminated from the parental strand via interactions between MMR proteins and the replisome.
Author: Martinus R. Schaaper
Publisher:
ISBN:
Category :
Languages : en
Pages : 106
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Author: Errol C. Friedberg
Publisher: American Society for Microbiology Press
ISBN: 1555813194
Category : Science
Languages : en
Pages : 2587
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Book Description
An essential resource for all scientists researching cellular responses to DNA damage. • Introduces important new material reflective of the major changes and developments that have occurred in the field over the last decade. • Discussed the field within a strong historical framework, and all aspects of biological responses to DNA damage are detailed. • Provides information on covering sources and consequences of DNA damage; correcting altered bases in DNA: DNA repair; DNA damage tolerance and mutagenesis; regulatory responses to DNA damage in eukaryotes; and disease states associated with defective biological responses to DNA damage.
Author: David Bramhill
Publisher:
ISBN:
Category :
Languages : en
Pages : 140
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Author: Grethe Evensen
Publisher:
ISBN:
Category :
Languages : en
Pages : 75
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This support summarizes studies on repair of methylmethane-sulfonate (MMS) alkylation lesions in DNA of the bacterium Escherichia coli. It shows that E. coli has two distinct 3-methyladenine (M3A) DNA glycosylase activities; one is constitutively expressed and encoded by the tag gene (TagI), whereas the other is inducible and encoded by alkA (TagII). The tag glycosylase is identified radiochemically as a 21 kdal protein whereas the alkA product is a 30 kdal protein. It is induced upon exposure of the cells to low levels of alkylating agents, a treatment that induces the adaptive response. TagII is not under control of recA, necessary to induce the mutagenic SOS response. TagI appears responsible for rapid repair of m3A alkylation products in unadapted cells. The inducible enzyme, TagII, is required for killing adaptation to alkylation resistance and for repair of potentially lethal lesions not recognized by the constitutive enzyme in unadapted cells. Persisting m3A alkylation products in DNA are shown to be cytotoxic for cells but not mutagenic. It is indicated that DNA glycosylases have a direct role in mutagenesis by creating AP-sites as premutagenic lesions, processed by the SOS system. Increased mutations in tag or alkA mutants can be ascribed to more rapid induction of the SOS response by persisting 3-methylpurines. Keywords: Genetics; Gene repair; Genes.
Author:
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Category :
Languages : en
Pages :
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Book Description
The subject of this thesis is repair of DMA damage in bacteria caused by ultraviolet irradiation and the errors made during this repair. In particular the study centred on post-replication repair. Two different approaches were used. First, genetical methods were used to study the effect of UV irradiation on mutation under varied conditions. Secondly, biochemical methods were used to examine changes in newly synthesized DNA under the same conditions. Thus, an attempt was made to correlate changes in the DNA with genetical changes. A survey of the most relevant literature is given in Chapter 1. Chapter 2 discusses materials and methods used. The rest of the thesis deals with results of experimental work. In Chapter 3 the effects of different post-irradiation treatments on mutation and repair are examined. The main conclusion is that the mutation enhancement caused by adding broth or acriflavine to post-irradiation medium cannot be entirely due to an effect on excision repair. In Chapter 4 a comparison is made between repair in excision deficientand excision proficient bacteria after low doses of UV irradiation. In Chapter 5 the relationship between the filling of daughter strand gaps and mutation fixation in an excision deficient strain is examined. It was discovered that under certain well-defined conditions gap filling was error-free. The sixth chapter deals with mutation frequency decline, or MFD. It was found that MFD could occur both pre- and post-replicatively and could thus not be explained solely as an effect on pre-replicative excision.
Author: David Mittelman
Publisher: Springer Science & Business Media
ISBN: 1461462800
Category : Medical
Languages : en
Pages : 284
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Book Description
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.
