Repair Replication Schemes in Bacteria and Human Cells

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The chapter discusses the schemes that remove damage from the DNA and attempt restoration of the original nucleotide sequence. The excision-repair of damaged DNA must involve a coordinated sequence of steps beginning with recognition of the lesion. After phosphodiester bonds are broken, the integrity of the interrupted DNA strand is restored through the enzymic processes of degradation, repair resynthesis, and ligation. Pathways for excision-repair in E.coli are elucidated through analysis of mutants deficient in various enzyme activities. A pathway mediated by DNA polymerase I that results in short repair patches approximately 20 nucleotides in extent; a pathway that results in a somewhat larger average patch size, probably due to intrinsic properties of DNA polymerases II and III; and a pathway that is induced in response to DNA damage and is dependent upon protein synthesis, requires recA+ and lexA+, and leads to much longer patches. Short patches are initiated and completed earlier than the long patches produced by the inducible pathway. In UV-irradiated human cells, only a single class of repair patches comparable in size to the short patches in E.coli, is synthesized at both early and late times after irradiation. The same patch size distribution also results from the treatment of human cells by angelicin or 8-methoxypsoralen plus long-wavelength UV, or by activated aflatoxin B1. © 1981, Academic Press Inc.




Hanawalt, P. C., Cooper, P. K., & Smith, C. A. (1981). Repair Replication Schemes in Bacteria and Human Cells. Progress in Nucleic Acid Research and Molecular Biology, 26(C), 181–196.

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