The roles of activin and follistatin signaling in chick gastrulation.

Abstract

Activin, a TGF-beta family member, and follistatin, an activin antagonist, encode signaling proteins which have been implicated in fundamental events in early vertebrate embryogenesis, such as mesoderm and neural tissue induction, and axial patterning. In this study I examine the roles of activin and follistatin in gastrulation in the chick. Activin betaB is found to be expressed at the base of the primitive streak prior to its formation, consistent with a role in streak induction. Follistatin has a more complex and dynamic expression in Hensen's node, and exhibits a left-right (LR) asymmetry. Antagonizing endogenous activin by ectopic application of follistatin protein causes the partial dissolution of the primitive streak and node, both morphologically and as assayed by loss of expression of molecular markers. This suggests that activin is necessary for the maintenance of streak morphology, and that follistatin may be involved in termination of the anterior progress of streak growth or in suppression of supernumerary streaks. Cell ingression through the node following follistatin application is normal, suggesting that it does not depend on the pit-like morphology of the wild-type node. Finally, follistatin temporally extends the asymmetric pattern of expression of HNF3-beta, this, as well as the stronger right-sided expression of follistatin, suggests a possible role in LR patterning.