Transcription-dependent and independent DNA excision repair pathways in human cells.
alpha-Amanitin, an inhibitor of RNA polymerase II, has little effect on either UV-induced incision or repair synthesis in cultured normal human fibroblasts but almost completely inhibits both processes in xeroderma pigmentosum group C fibroblasts. Cycloheximide, at a concentration which inhibits protein synthesis by 75-80%, has no effect on incision or repair synthesis in either cell type, which argues that the effects of alpha-amanitin on repair occur at the level of transcription. Cot analysis demonstrates that UV-induced repair synthesis occurs at similar levels in highly repetitive, middle repetitive and single copy sequence in both normal and xeroderma group C cells. We conclude that normal cells must have at least two excision repair pathways for repair of UV-induced damage, one dependent on transcription and the other independent.
Carreau
M
M
Department of Nuclear Medicine and Radiobiology, Faculty of Medicine, Université de Sherbrooke, Que., Canada.
Hunting
D
D
D000546:Amanitins / Q000494:pharmacology*; D002478:Cells, Cultured; D003513:Cycloheximide / Q000494:pharmacology; D004247:DNA / Q000096:biosynthesis* / Q000235:genetics / Q000528:radiation effects; D004260:DNA Repair / Q000187:drug effects*; D006801:Humans; D012091:Repetitive Sequences, Nucleic Acid / Q000235:genetics; D014158:Transcription, Genetic / Q000235:genetics*; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000235:genetics* / Q000378:metabolism
D000546:Amanitins; D004247:DNA; D003513:Cycloheximide