Pax genes encode DNA binding proteins that play pivotal roles in the 
determination of complex tissues. Members of one subclass, Pax6, function as 
selector genes and play key roles in the retinal development of all seeing 
animals. Mutations within the Pax6 homologs including fly eyeless, mouse Small 
eye and human Pax6 lead to severe retinal defects in their respective systems. 
In Drosophila eyeless and twin of eyeless, play non-redundant roles in the 
developing retina. One particularly interesting characteristic of these genes is 
that, although expression of either gene can induce ectopic eye formation in 
non-retinal tissues, there are differences in the location and frequencies at 
which the eyes develop. eyeless induces much larger ectopic eyes, at higher 
frequencies, and in a broader range of tissues than twin of eyeless. In this 
report we describe a series of experiments conducted in both yeast and flies 
that has identified protein modules that are responsible for the differences in 
tissue transformation. These domains appear to contain transcriptional activator 
and repressor activity of distinct strengths. We propose a model in which the 
selective presence of these activities and their relative strengths accounts, in 
part, for the disparity to which ectopic eyes are induced in response to the 
forced expression of eyeless and twin of eyeless. The identification of both 
transcriptional activator and repressor activity within the Pax6 protein 
furthers our understanding of how this gene family regulates tissue 
determination.