Postreplication repair of DNA in chick cells: studies using photoreactivation.
During replication of DNA after ultraviolet irradiation, gaps are left in the newly-synthesized DNA strands in both bacterial and animal cells and these gaps are subsequently sealed by a process known as postreplication repair. In order to test whether it is the ultraviolet-induced pyrimidine dimers which are responsible for the production of these daughter-strand gaps in animal cells, we have used chick embryo fibroblasts. In these cells the pyrimidine dimers are photoreactivable, i.e. they can be split by an enzymatic process dependent on visible or near ultraviolet light. Our results indicate that chick cells possess a postreplication repair system similar to that in mammalian cells; gaps are produced in the newly-synthesized strands and then filled in. If the ultraviolet-irradiated cells are first photoreactivated to remove most of the dimers, the number of daughter-strand gaps produced is much less than without photoreactivation. This suggests that the dimers are indeed responsible for the formation of many of the gaps in the newly-synthesized DNA. Ultraviolet light also inhibits the overall rate of DNA synthesis. This inhibition is, however, only partly overcome by photoreactivation.
D000818:Animals; D002642:Chick Embryo; D004260:DNA Repair / Q000528:radiation effects*; D004261:DNA Replication / Q000528:radiation effects*; D004720:Endonucleases; D007700:Kinetics; D008027:Light; D008836:Micrococcal Nuclease; D010777:Photochemistry; D011742:Pyrimidine Nucleotides; D011830:Radiation Effects; D013936:Thymidine / Q000378:metabolism; D014466:Ultraviolet Rays
D011742:Pyrimidine Nucleotides; D004720:Endonucleases; D008836:Micrococcal Nuclease; D013936:Thymidine