Modification and Repair of Alkylation-induced Mutagenesis in "Escherichia Coli" PDF Download
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Author: Angela Mary Keogh
Publisher:
ISBN:
Category :
Languages : en
Pages : 558
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Author: Angela Mary Keogh
Publisher:
ISBN:
Category :
Languages : en
Pages : 558
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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: Grethe Evensen
Publisher:
ISBN:
Category :
Languages : en
Pages : 148
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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.
Author: Kristin A. Eckert
Publisher:
ISBN:
Category :
Languages : en
Pages : 418
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Author: G. Evensen
Publisher:
ISBN:
Category :
Languages : en
Pages : 74
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Author:
Publisher:
ISBN:
Category :
Languages : en
Pages : 500
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Author: Martinus R. Schaaper
Publisher:
ISBN:
Category :
Languages : en
Pages : 106
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Author: Alexis Ann Johnson
Publisher:
ISBN:
Category :
Languages : en
Pages : 122
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Author: Andrei Kuzminov
Publisher: Landes Bioscience
ISBN:
Category : Medical
Languages : en
Pages : 234
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