Fig. 2. Retinal defects following UV irradiation are due to DNA damage. (A) Irradiation of 24 h APF retinae resulted in a rapid induction of pyrimidine dimers. Each four-cell group is the cone cell nuclei of one ommatidium; an example is circled. The inset presents a non-irradiated control. (B) Exposure of the retina to light 2 h after irradiation resulted in a complete suppression of the UV retinal phenotype due to photoreactivation- mediated repair of the pyrimidine dimers. (C) Photoreactivating light failed to fully rescue the retina when applied 7 h after irradiation. (D) A deficiency removing the 29–30C region of the second chromosome strongly enhanced the UV phenotype (compare with Figure 1B). This region is predicted to contain xpg/mus201, along with a number of other loci. (E) Removing both functional copies of the nucleotide excision repair gene xpg/mus201, using the mus201^D1 allele, resulted in a complete ablation of the retina following irradiation. The dying pupa was removed from its pupal case; few structures are identifiable as the entire retina and much of the head is affected. (F) A frontal view of this animal reveals the extent of the damage. The non-irradiated retina showed no defects. A comparison of TUNEL staining in wild type (G) and the xpg/mus201^D1 mutant (H) revealed that the xpg/mus201 phenotype was due to a dramatic increase in apoptotic cell death (42 h APF). (I) Exposure of the xpg/mus201^D1 retina to light following irradiation resulted in suppression of the lethality as well as retinal and head defects.