Exposure to ultraviolet radiation causes apoptosis in developing sea urchin embryos

Abstract

SUMMARYLaboratory 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.

Physiological adaptation to Mediterranean habitats of the native crab <em>Pachygrapsus marmoratus</em> and the invasive <em>Percnon gibbesi</em> (Crustacea: Decapoda)

“…In fact, exposure to UV radiation and ROS can act synergistically to cause extensive DNA damage and lead to apoptosis (Lesser et al 2001). Inadequate protection against UV radiation and ROS may result in damage to DNA, proteins and membrane lipids that will compromise the physiology and biochemistry of the organisms (Lesser et al 2003). Consequently, the content of vitamin E in P. marmoratus should be higher to protect against oxidation and UV radiation as an adaptation to the supralittoral environment.…”

Exposure to Ultraviolet Radiation Causes Proteomic Changes in Embryos of the Purple Sea Urchin, Strongylocentrotus Purpuratus

“…Exposure to UVB radiation results in direct protein damage by photochemical degradation of tryptophan and tyrosine residues and destroys disulfide bonds required for proteinprotein interactions (Hollósy, 2002;Tevini 1993). UVB damages DNA through the production of cyclobutane pyrimidine dimers (CPD's) among other photoproducts (Imlay and Linn, 1988;Lesser et al, 2003;Peak and Peak, 1990;Setlow 1974;Tevini 1993). UVA makes up greater than 90% of the total UVR that reaches Earth's surface and causes photooxidative damage through the production of reactive oxygen species (ROS) that rapidly oxidize nucleic acids, proteins and lipids (Pourzand and Tyrrell, 1999;Tyrrell 1991).…”

“…Sea urchins inhabit all of Earth's major oceans and have developmental stages sensitive to UVR (Adams and Shick, 1996;Anderson et al, 1993;Lesser et al, 2003). Many live intertidally and broadcast spawn gametes that initially sink.…”

“…Sea urchin embryos also sustain UV-induced DNA damage (Lesser et al, 2003;2006). Common repair mechanisms utilized by cells in aquatic organisms are base excision repair (BER), nucleotide excision repair (NER), and mismatch repair for single-stranded breaks and homologous or non-homologous recombination for double stranded breaks (Sinha and Häder, 2002).…”

“…Photoreactivation involves the use of UVA and photosynthetically active radiation (PAR, 401-700 nm) energy to activate photolyase, which splits DNA dimers created by UVR (Häder et al, 2007;Thoma, 1999). Importantly, studies have specifically documented the production of CPD's and photorepair in UVR stressed embryos (Akimoto and Shiroya, 1987;Lesser et al, 2003;2006).…”