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 increased by the depletion of the ozone layer. We have examined the genotoxicity of solar ultraviolet, especially the longer wavelengths light, using Drosophila. Recently, we have demonstrated that light of wavelengths up to 340 nm 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 310 nm, and that light of 330 and 340 nm may induced damage different from that induced by 310 and 320 nm-light. To examine the difference in DNA damage induced by light of particular wavelength, we performed monochromatic irradiation on larvae of two Drosophila strains; one excision repair-deficient (mei-9) and another postreplication repair-deficient (mei-41). 310 and 320 nm-light was more mutagenic in the mei-9 strain than mei-41, whereas 330 and 340 nm-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 3300-360 nm-light causes damage to be recognized by the cell cycle checkpoint but it is not repairable by NER

Somatic cell mutation and photoproduct formation in Drosophila induced by monochromatic UV light in sunlight

We recently reported that natural sunlight can induce somatic mutation and chromosomal recombination in Drosophila, as detected by the wing spot test. Simultaneously, cyclobutane thymine dimers (CTDs) and (6-4)photoproducts [(6-4)PPs] are formed in the DNA. In the present work, we have performed monochromatic UV irradiation for evaluating the action spectrum of sunlight in genotoxicity. Third instar larvae in petri dishes were irradiated by monochromatic UV light at a wavelength between 310 and 360 nm. The mutant spots induced by the irradiation of 310, 320, 330, and 340 nm light were (4.4 ± 1.0) x 10 -1, (1.1 ± 0.2) x 10 -2, (2.5 ± 0.7) x 10 -3, and (2.0 ± 0.7) x 10 -3 spots/wing/kJ/m 2, respectively. The mutagenicity at 360 nm irradiation was not significant. The amounts of photoproducts in irradiated larval DNA were measured by an enzyme-linked immunosorbent assay (ELISA) using the monoclonal antibodies against CTDs and (6-4)PPs. CTDs were found in the DNA from all of these irradiated larvae, and their amounts increased with the UV dose: the longer the wavelength, the lower the CTD formation and the mutagenesis. These data suggest that, in the sunlight, the component around 310-340 nm causes the somatic cell mutation by forming thymine dimers as main lesions