Work from a number of laboratories recently has demonstrated that alterations in chromatin structure occur during excision repair in mammalian cells. It is now clear that when cells are damaged with a wide variety of chemical agents or ultraviolet radiation, almost all of the repair synthesis is initially sensitive to staphylococcal nuclease. With time, there is a redistribution of the counts incorporated during excision repair synthesis so that many of them become nuclease resistant and associated with nucleosome core length DNA. In our laboratory, we have demonstrated this phenomenon in human cells damaged with N-acetoxy-2-acetylaminofluorene, 7-bromomethylbenz[a]anthracene, and ultraviolet radiation. It is clear from the work of others that the phenomenon is not unique to human cells since African green monkey cells damaged with either ultraviolet radiation or angelicin also show an initial nuclease sensitivity of repair-incorporated nucleotides follow by rearrangement. Two models to explain these observations have been proposed; one suggests that there is an unfolding of nucleosomes during excision repair followed by a refolding, while the other suggests that sliding of core proteins with respect to DNA occurs during excision repair. These models, as well as recent data bearing on them, will be discussed.
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