Rearrangement of mammalian chromatin structure following excision repair: absence of an effect of inhibitors of poly (ADP-ribose) polymerase and topoisomerase.
Newly-repaired DNA in chromatin is more sensitive to micrococcal nuclease than bulk DNA, but tends to become equally sensitive with time. This rearrangement of chromatin, which had previously been observed following repair of lesions produced by UV-light and of some bulky adducts, has now been shown to occur after repair of lesions induced by hydrogen peroxide and dimethylsulfate. In both cases there was an enhanced sensitivity to nuclease digestion of newly repaired DNA followed by a rearrangement whose kinetics was very similar to that observed in UV irradiated cells. Benzamide and 3-aminobenzamide, inhibitors of the synthesis of poly (ADP-ribose) and novobiocin, an inhibitor of topoisomerase, had no effect on the initially enhanced digestibility of repaired regions or on the chromatin rearrangement that followed. Poly (ADP-ribose) polymerase and topoisomerase are known to play some role in excision repair and have also been shown to cause alterations in the chromatin structure. However, the present results show that these alterations are not involved in this kind of chromatin rearrangement.
D001549:Benzamides / Q000494:pharmacology; D002843:Chromatin / Q000648:ultrastructure*; D004247:DNA / Q000528:radiation effects; D004260:DNA Repair / Q000187:drug effects*; D006801:Humans; D008836:Micrococcal Nuclease / Q000378:metabolism; D009675:Novobiocin / Q000494:pharmacology; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D013997:Time Factors; D059005:Topoisomerase II Inhibitors; D014466:Ultraviolet Rays
D001549:Benzamides; D002843:Chromatin; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D059005:Topoisomerase II Inhibitors; D009675:Novobiocin; C025160:3-aminobenzamide; D004247:DNA; D008836:Micrococcal Nuclease