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These changes, each of which reflects more or less severe cellular stress, include cycle delay, chromosome behaviour, fall in NAD level, the development of double-stranded DNA breaks, rapid chromosome fragmentation and cell killing. Disruption of the repair process by agents such as araC after therapeutic DNA damage may, therefore, have some potential value in cancer treatment. The extreme cellular problems associated with the artificial arrest of repair may have their subtler counterparts elsewhere, and we discuss several systems where delays in the completion of excision repair in the absence of repair synthesis inhibitors have marked repercussions on cell viability. We also show that the average completion time of an excision repair patch varies according to the state of cell culture, and that completion time is extended after treatment with insulin or following trypsin detachment. Under certain growth conditions ultraviolet irradiation followed by mitogenic stimulation results in double-stranded DNA breakage and additional cell killing, and we discuss these data in the light of protocols that have been used successfully to transform human or rodent cells in vitro. Finally, we consider whether the rejoining of DNA breaks accumulated by repair synthesis inhibitors is a valid model system for studying ligation, and show that this protocol provides an extremely sensitive assay for most incision events and, thereby, a means for discriminating between normal human cells on the one hand, and Cockayne\u2019s Syndrome cells and their heterozygotes on the other.<\/jats:p><jats:p>\u2021Present address: Genetics Institute, Biological Research Center, Hungarian Academy of Sciences, P.O.B. 501, Szeged, Hungary.<\/jats:p>","DOI":"10.1242\/jcs.1984.supplement_6.18","type":"journal-article","created":{"date-parts":[[2013,5,23]],"date-time":"2013-05-23T07:59:48Z","timestamp":1369295988000},"page":"263-288","source":"Crossref","is-referenced-by-count":16,"title":["DNA Repair Under Stress"],"prefix":"10.1242","volume":"1987","author":[{"given":"R. T.","family":"Johnson","sequence":"first","affiliation":[{"name":"Cancer Research Campaign Mammalian Cell DNA Repair Group, Department of Zoology, Cambridge University, Downing Street, Cambridge CB2 3EJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. R. S.","family":"Collins","sequence":"additional","affiliation":[{"name":"Cancer Research Campaign Mammalian Cell DNA Repair Group, Department of Zoology, Cambridge University, Downing Street, Cambridge CB2 3EJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shoshana","family":"Squires","sequence":"additional","affiliation":[{"name":"Cancer Research Campaign Mammalian Cell DNA Repair Group, Department of Zoology, Cambridge University, Downing Street, Cambridge CB2 3EJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ann M.","family":"Mullinger","sequence":"additional","affiliation":[{"name":"Cancer Research Campaign Mammalian Cell DNA Repair Group, Department of Zoology, Cambridge University, Downing Street, Cambridge CB2 3EJ, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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