Photoreactivation rescue and hypermutability of ultraviolet-irradiated excisionless Drosophila melanogaster larvae

• Published in: Proceedings of the National Academy of Sciences - PNAS 1986-05, Vol.83 (10), p.3366-3370
• Main Authors: Ryo, H, Kondo, S
• Format: Article
• Language: English
• Subjects: Age Factors; Animals; Biological and medical sciences; Biological Sciences: Genetics; Deoxyribodipyrimidine Photo-Lyase - metabolism; Dimers; DNA damage; DNA repair; DNA Repair - radiation effects; DNA Replication; Drosophila; Drosophila melanogaster; Drosophila melanogaster - genetics; Fundamental and applied biological sciences. Psychology; gene expression; Genetic mutation; Insect larvae; Instars; Irradiation; Larva; Larvae; Light; Lyases - metabolism; Molecular and cellular biology; Molecular genetics; Mutagenesis. Repair; Mutation - radiation effects; Pyrimidine dimers; radiation injuries; repairing; somatic mutation; ultraviolet radiation; Ultraviolet Rays; X-Rays
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.83.10.3366

There is accumulating evidence suggesting that expression of genes for repair of UV damage to DNA in mammals and fish is regulated developmentally. Therefore, the activity of excision repair and photoreactivation in vivo in young larvae of Drosophila melanogaster was examined in a strain carrying the mutation mus201 that was unable to carry out excision repair. The photoreactivation activity in firstinstar larvae was so high that UV-induced lethality in excisionless larvae was almost completely rescued by posttreatment with fluorescent light. Excision repair activity in first-instar repair-proficient larvae was so high that UV irradiation was scarcely able to produce somatic eye-color mutations. In contrast, excisionless larvae showed a high incidence of somatic eye-color mutation after UV-irradiation, and this incidence was reduced to the spontaneous level by posttreatment with fluorescent light. Incorporation of a postreplication repair-defective mutation into the excisionless strain decreased the incidence of UV-induced somatic mutations by a factor of 3. The analogous repair dependence of UV mutagenesis in Drosophila and Escherichia coli is discussed. It is proposed that UV-induced somatic mutations in excisionless Drosophila larvae are caused primarily by pyrimidine dimers and that a constitutive, error-prone pathway for filling daughter-strand gaps opposite dimers is, at least partly, responsible for the fixation of mutations.