Loss of Pax 6 function leads to an eyeless phenotype in both mammals and 
insects, and ectopic expression of both the Drosophila and the mouse gene leads 
to the induction of ectopic eyes in Drosophila, which suggested to us that Pax 6 
might be a universal master control gene for eye morphogenesis. Here, we report 
the reciprocal experiment in which the RNAs of the Drosophila Pax 6 homologs, 
eyeless and twin of eyeless, are transferred into a vertebrate embryo; i.e., 
early Xenopus embryos at the 2- and 16-cell stages. In both cases, ectopic eye 
structures are formed. To understand the genetic program specifying eye 
morphogenesis, we have analyzed the regulatory mechanisms of Pax 6 expression 
that initiates eye development. Previously, we have demonstrated that Notch 
signaling regulates the expression of eyeless and twin of eyeless in Drosophila. 
Here, we show that in Xenopus, activation of Notch signaling also induces 
eye-related gene expression, including Pax 6, in isolated animal caps. In 
Xenopus embryos, the activation of Notch signaling causes eye duplications and 
proximal eye defects, which are also induced by overexpression of eyeless and 
twin of eyeless. These findings indicate that the gene regulatory cascade is 
similar in vertebrates and invertebrates.