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Clues to the Organization of DNA Repair Systems Gained from Studies of Intragenomic Repair Heterogeneity

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Advances in Mutagenesis Research

Part of the book series: Advances in Mutagenesis Research ((MUTAGENESIS,volume 1))

Abstract

The investigation of DNA repair processes in mammalian cells has largely been modeled upon results obtained with prokaryotes, most notably E. coli. The general aspects of the organization and functioning of a number of repair systems in mammalian cells do indeed appear to be rather similar to those in prokaryotes (Friedberg 1984). Both utilize: (1) a broad-spectrum excision repair system that recognizes and removes a variety of bulky, DNA-distorting lesions; (2) many individual glycosylases that specifically remove a variety of altered or damaged bases to produce repairable abasic sites; and (3) systems for directly reversing certain lesions like 0-6-alkyl guanine. Although the strategies used may not be identical, both eukaryotes and prokaryotes have been shown to repair mismatches and double-strand breaks, and to possess tolerance mechanisms to facilitate the replication of DNA containing lesions (sometimes termed postreplication repair).

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Abbreviations

4NQO:

4-nitroquinoline 1-oxide

ADA:

adenosine deaminase

BrUra:

5-Bromo-2’-deoxyuracil

CHO:

Chinese hamster ovary

CS:

Cockayne’s syndrome

DHFR:

dihydrofolate reductase

HPRT:

hypoxanthine-guanine phosphoribosyl transferase

kb:

kilobases

MHC:

major histocompatpatibility

MT:

metallothionein

PD:

cyclobutyl pyrimidine dimer(s)

TEV:

T4 endonuclease V

XP:

xeroderma pigmentosum

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Smith, C.A., Mellon, I. (1990). Clues to the Organization of DNA Repair Systems Gained from Studies of Intragenomic Repair Heterogeneity. In: Obe, G. (eds) Advances in Mutagenesis Research. Advances in Mutagenesis Research, vol 1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74955-1_6

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