Protein tyrosine kinase activity following fertilization is required to complete gastrulation, but not for initial differentiation of endoderm and mesoderm in the sea urchin embryo

Abstract

The egg activation process functions to implement developmental programs that act much later in embryogenesis. One example of this is the fact that application of protein tyrosine kinase inhibitors to the fertilized sea urchin egg for a 15-min period results in a defect in the gastrulation process occurring over 24 h later (Kinsey, W. H., Der. Biol. 172, 704-707, 1995). In the present study, we show that the window of sensitivity is not due to differential uptake of inhibitor, and establish that the inhibitor inhibits tyrosine kinase activity at the time of application. We also demonstrate that inhibition of protein tyrosine kinase activity in the zygote causes a specific defect in the morphogenetic movements associated with gastrulation without interfering with the initial specification and differentiation of endoderm and mesoderm. Differentiation events occurring concurrent with or subsequent to gastrulation were also suppressed in embryos derived from treated zygotes. These findings indicate that fertilization initiates a signaling cascade involving protein tyrosine kinase activity that is required specifically for events at gastrulation. This signaling event is required to complete the developmental program of both endoderm and mesoderm, but is different from those events necessary for initial specification of endodermal and mesodermal cell fate.