Stress-induced apoptosis in sea urchin embryogenesis

We find that early sea urchin embryos have the capability to induce programmed cell death, or apoptosis, in response to chemical and physical stress. Strongylocentrotus purpuratus embryos (fertilized, 4 cell, 16 cell, 64 cell, and early blastula) were exposed to known cytotoxins, in order to determine when apoptosis occurs naturally and in response to stress. Using cell permeability as an indicator of early stage apoptosis, caspase activation as a mid-stage indicator, and DNA fragmentation as a late stage indicator, we find that during the cleavage stage of embryogenesis apoptosis is almost completely absent. However, a statistically significant (p<0.001) rise in apoptosis in stressed embryos is evident around 24 h after fertilization, during the early blastula stage and shortly after hatching. Before this stage, exposed embryos show no statistically significant increases in apoptosis in comparison to the controls. This pattern of apoptosis in development is similar to that seen in lower vertebrate models in which stress-induced apoptosis occurs only around the mid-blastula transition. We conclude that apoptosis may be used to rid embryos of aberrant or damaged cells in early development, but this response is stage-dependant. Repair, rather than apoptosis, may be utilized during earlier stages, or alternatively, embryos exposed to such stressors may continue development with damaged cells and perhaps damaged DNA. Our continued studies will focus on these alternative hypotheses.