Such a phenotype could be a powerful tool in the further exploration of mechanisms that control regeneration. And many questions about these mechanisms remain.
"For example, the animals know how far to grow in regeneration, so they don't make tumorous outgrowths," says Wenemoser, who is now a postdoctoral researcher at Stanford University. "There's some kind of regulation on homeostatic size, so they're not growing out all wild and crazy. There's definitely more to investigate there."
Gavio agrees, and points out that the fst/act-1/2 switch may ultimately help scientists tease apart regeneration in other organisms, including humans.
"This regulation by activin and follistatin may be conserved in other systems," says Gavio, who is currently a postdoctoral researcher at Univeristy of California, San Francisco. "There are a lot of hints in the scientific literature that versions of activin or follistatin or both are activated by injury and may play a role in regeneration in other animals, but pinning the role of initiating regeneration to them hasn't happened yet."
|Contact: Nicole Rura|
Whitehead Institute for Biomedical Research