Abstract
Much of our basic understanding of cellular repair mechanisms began with a thorough analysis of the processing of cyclobutane pyrimidine dimers in the DNA of Escherichia coli (6, 7). Furthermore, it is now well-documented in this Volume that there are still important discoveries to be made using bacteria as model systems for studying the mechanisms of antimutagenesis. The recent advances in our understanding of DNA damage processing in E. coli attest to the complexity of such mechanisms in even the simplest prokaryote systems (15). These advances include the discovery of new inducible responses to lesions in DNA, new insights into the mechanism of mismatch repair, and the development of defined sequence DNA probes for assessing the molecular spectrum of mutagenic actions. It is essential that basic research on important prokaryote model systems continues to receive adequate emphasis and support even though our long-term goal may be to understand the mechanisms of antimutagenesis and anticarcinogenesis in humans. The results from research on E. coli still serve to guide our exploration of DNA damage processing in mammalian cells (4, 10).
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References
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© 1986 Plenum Press, New York
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Hanawalt, P.C. (1986). Introduction: Comparative Responses to DNA Damage in Bacteria and Mammalian Cells. In: Shankel, D.M., Hartman, P.E., Kada, T., Hollaender, A., Wilson, C.M., Kuny, G. (eds) Antimutagenesis and Anticarcinogenesis Mechanisms. Basic Life Sciences, vol 39. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5182-5_24
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DOI: https://doi.org/10.1007/978-1-4684-5182-5_24
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