Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos.

Laboratory exposures of embryos from the sea urchin Strongylocentrotus droebachiensis to ultraviolet B radiation (UV-B, 290-320 nm), equivalent to a depth of 1-3 m in the Gulf of Maine, resulted in significant damage to DNA measured as cyclobutane pyrimidine dimer formation. Cells with DNA damage caused by ultraviolet radiation (UVR, 290-400 nm) and oxidative stress can survive, but are often retained in the G1/S phase of the cell cycle to repair DNA as a result of the expression of cell cycle genes such as p53 and p21, and the subsequent inhibition of the activity of cyclin-dependent kinases such as cdc2; if DNA cannot be repaired it can lead to programmed cell death or apoptosis. Sea urchin embryos exposed to UV-B radiation exhibit significantly higher protein concentrations of the antioxidant enzyme superoxide dismutase, and the transcriptional activators p53 and p21. The downstream activator of the cell cycle, cdc2, showed significantly lower protein concentrations with exposure to increasingly shorter wavelengths of UVR. Decreases in cdc2 could have been caused directly by exposure to UV-B or as a result of downregulation via the p53, p21 cascade, or both. These cellular events lead to apoptosis, as shown by the significant increase in DNA strand breaks observed in the nuclei of developing embryos exposed to UVR using the TUNEL assay. Cellular death, and a decrease in sea urchin embryo survivorship, are caused by the indirect and direct effects of exposure to UVR that leads to apoptosis in these laboratory experiments.