Stanford Today Edition: May/June, 1998 Section: Science and Medicine: Tough Embryos WWW: Tough Embryos
Science and Medicine News
The majority of living organisms start out life unprotected by a womb or a nest in the soil or the sea, under broiling heat or in contaminated waters, yet they manage to survive and grow to adulthood.
For years, Stanford marine biologist David Epel has been intrigued by the enigma of the embryo. This is the most fragile stage of life, little more than a bare cluster of rapidly dividing cells dedicated to building a sea urchin or a fish or a mouse. For that reason he and James Clegg from the University of California-Davis decided to lead the first symposium to discuss the strategies that embryos use to survive.
"We know surprisingly little at the cellular and molecular level about how embryos cope with their environments, yet the embryo's survival is critical for sustaining the life of a species," said Epel, professor of biological sciences at the Hopkins Marine Station.
At the symposium during the annual meeting of the American Association for the Advancement of Science, Joseph Kiesecker, a postdoctoral fellow at Yale, described how DNA damage to developing frogs' eggs, caused by a dose of ultraviolet-B light, can make the eggs vulnerable to a deadly fungus. Over the past decade, scientists worldwide have noticed a decline in the populations of frogs and many other species of amphibians; some think that a contributing factor may be the thinning ozone layer in the atmosphere, which could expose amphibians' eggs to extra doses of DNA-harming UV-B light. Kiesecker found a rescue mechanism that frog embryos evolved eons ago to repair DNA damage. The gene repair work is done by an enzyme called photolyase, and frog eggs from species with the greatest photolyase activity are most likely to survive a blast of UV-B light and less likely to succumb to later assaults by the fungus.
Roger Pedersen, research director of the reproductive genetics unit at the University of California-San Francisco, reported that mouse embryos use one type of DNA repair, called base excision repair, as part of a mechanism to cope with DNA damage or to initiate a "self-destruct" program if the harm cannot be repaired.
In his own research, Epel has found a coping mechanism that embryos use to prevent damage before it has to be repaired - an essential protection for a species like the fat innkeeper worm, which survives in coastal mudflats by resisting natural and man-made toxins. The innkeeper worm's embryo detects toxins as soon as they touch a cell wall and spits them out. This defense, evolved over millennia, depends on a protein in the cell wall called a multi-drug transporter. The same protein in human cells sometimes leads to less happy consequences - when a tumor uses multi-drug transporter proteins to spit out anti-cancer drugs.
The different studies show that most organisms have built-in mechanisms to survive insults from their environments. In embryos, these mechanisms often are different than in adults, Epel said. "One reason is that the embryo has not developed the adult's mechanisms for coping. It is adapted to a particular niche and to a particular task - rapid cell division and development," and each organism's embryos probably rely on more than one protective mechanism.