The involvement of cell cycle checkpoint-mutations in the mutagenesis induced in Drosophila by a longer wavelength light band of solar UV

Solar ultraviolet radiation is considered to be injurious rather than necessary for most organisms living on the earth. It is reported that the risk of skin cancer in humans increases by the depletion of the ozone layer. We have examined the genotoxicity of solar ultraviolet, especially the longer wavelength light, using Drosophila. Recently, we have demonstrated that light of wavelength up to 340 rim is mutagenic on Drosophila larvae. Using an excision repair-deficient Drosophila strain (mus201), we have obtained results suggesting that the lesion Caused in larvae by the 320 nm-light irradiation may be similar to the damage induced by irradiation at 3 10 nm, and that light of 330 and 340 urn may induce damage different from that induced by 3 10 and 320 rim-light. To examine the difference in DNA damage induced by light of a particular wavelength, we performed monochromatic irradiation on larvae of two Drosophila strains; one excision repair-deficient (mei-9) and another post replication repair-deficient (mei-41). 3 10 and 320 nm-light was more mutagenic in the mei-9 strain than in mei-41, whereas 330 and 340 run-light was more mutagenic in mei-41 than in mei-9. It is demonstrated that the mei-41 gene is a homologue of the human atm gene which is responsible for a cell cycle checkpoint. This result suggests that 310-320 nm-light induces DNA damage that is subject to nucleotide excision repair (NER) and that 330-360 nm-light causes damage to be recognized by the cell cycle checkpoint but it is not repairable by NER.