This chapter describes the details of the enzymic mechanisms of excision repair of damaged DNA. It is the incision of UV irradiated DNA by an enzyme mechanism, involving a specific DNA glycosylase that is not universal. This argument notwithstanding, even in the two biological systems just mentioned, evidence indicates that pyrimidine dimers are excised from DNA as a part of a larger oligonucleotide, whereas in all known examples of base-excision repair, the products of excision are free bases. The chapter also describes an activity in extracts of M. luteus that recognizes 8-(2-hydroxyisopropy1) purines in DNA. Preliminary evidence indicates that this activity is a true endonuclease without associated DNA glycosylase activity. Thus, it is distinctly possible that the excision repair of cell damage by hydrolysis of N-glycosyl bonds involves a number of specific forms of base damage, in which the degree of structural distortion of DNA secondary structure is limited. Very bulky DNA adducts such as those produced by the interaction of DNA with polycyclic aromatic hydrocarbons, acetamidofluorene, etc., may generate relatively nonspecific but significant distortion of the DNA helix that is recognized by a limited number of “general” endonucleases.
|Original language||English (US)|
|Number of pages||19|
|Journal||Progress in Nucleic Acid Research and Molecular Biology|
|State||Published - Jan 1 1981|
ASJC Scopus subject areas
- Molecular Biology