Rearrangement of mammalian chromatin structure following excision repair.

Abstract

Repair of DNA damage in eukaryotic cells involves local disruption of chromatin structure such that repair-incorporated nucleotides are transiently highly sensitive to digestion by staphylococcal nuclease (SN)1–4. We have examined the dependence of this phenomenon on the initial distribution in chromatin of DNA damage by comparing the repair of pyrimidine dimers, which are distributed randomly in chromatin5, with the repair of angelicin photoadducts, which are formed primarily in linker regions of nucleosomes6,7. We find that the transient nuclease sensitivity of repair patches is independent of the initial distribution of DNA damage in chromatin. In addition, our observation that repair patches produced in response to a linker-specific damaging agent become distributed randomly in chromatin implies that nucleosome cores do not necessarily return to their original sites along a DNA strand after the DNA is repaired.