Dmp53 protects the Drosophila retina during a developmentally regulated DNA damage response

• Published in: The EMBO journal Vol. 22; no. 20; pp. 5622 - 5632
• Main Authors: Cagan, Ross L, Jassim, Omar W, Fink, Jill L
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 15-10-2003; Blackwell Publishing Ltd; Oxford University Press
• Subjects: Animals; Apoptosis; Deoxyribonucleic acid; Diap1 protein; Dmp53; DNA; DNA Damage; Drosophila; Drosophila melanogaster; Drosophila Proteins - physiology; Hid protein; In Situ Nick-End Labeling; Microscopy, Electron, Scanning; Mortality; Pupa - radiation effects; Reaper protein; retina; Retina - physiology; Retina - radiation effects; Retina - ultrastructure; Trans-Activators - physiology; Tumor Suppressor Protein p53; Ultraviolet Rays
• ISSN: 0261-4189; 1460-2075; 1460-2075
• DOI: 10.1093/emboj/cdg543

Ultraviolet (UV) light is absorbed by cellular proteins and DNA, promoting skin damage, aging and cancer. In this paper, we explore the UV response by cells of the Drosophila retina. We demonstrate that the retina enters a period of heightened UV sensitivity in the young developing pupa, a stage closely associated with its period of normal developmental programmed cell death. Injury to irradiated cells included morphology changes and apoptotic cell death; these defects could be completely accounted for by DNA damage. Cell death, but not morphological changes, was blocked by the caspase inhibitor P35. Utilizing genetic and microarray data, we provide evidence for the central role of Hid expression and for Diap1 protein stability in controlling the UV response. In contrast, we found that Reaper had no effect on UV sensitivity. Surprisingly, Dmp53 is required to protect cells from UV‐mediated cell death, an effect attributed to its role in DNA repair. These in vivo results demonstrate that the cellular effects of DNA damage depend on the developmental status of the tissue.