EPEL, D.: The Uniqueness of Early Development: The Puzzling Response of Embryos to Environmental Insults

Studies on adult somatic cells have provided paradigms about cellular activities such as signal transduction, gene expression and responses to stress and repair of cell damage. The same activities also take place in embryos. But are the principles derived from studies on somatic cells relevant to embryos? Or are there unique, special characteristics of the embryonic state? One obvious singularity is totipotency but there are others that are not widely appreciated and provide insights for understanding how embryos work and develop. One unique property of the embryo is the robustness and canalization of early development with standardized outcome. Part of this robustness ensues from multiple or redundant pathways and also from protective measures to insure that DNA is not damaged as by UV or chemical mutagens. Yet this apparent robustness contrasts with research on embryos showing that some embryos do not repair DNA damage during cleavage and similarly do not synthesize heat shock proteins in response to physical or chemical insults. Both of these reparative abilities are suddenly acquired at the blastula stage. At about the same time there is also a burst of apoptosis, which removes cells that were severely damaged earlier during the cleavage period. What is the rationale for this absence of repair responses until the blastula stage? And why the sudden onset of apoptosis at this time? Is lack of repair, which will require more time, related to a need for rapid cleavage and quick attainment of a safer motile stage? Is postponement of apoptosis because all cells need to be present to facilitate accurate transfer of information as occurs in embryonic induction? Or does the absence of repair during cleavage lead to generation of genetic variation that can then be acted upon by natural selection?