“…For example, Pax2 null Zebrafish noi mutants fail to develop an isthmus (Brand et al, 1996), while Pax3 mutants have significant neural crest and neural tube/CNS defects (Auerbach, 1954;Wildhardt et al, 1996) and Pax5 knockout mice exhibit defects in the midbrain-hindbrain region (Urbanek et al, 1994(Urbanek et al, , 1997. Similarly, Pax6 mutations result in severe defects in forebrain development and eye formation (Hill et al, 1991;Jordan et al, 1992;Callaerts et al, 1997;Mastick et al, 1997;Niimi et al, 1999Niimi et al, , 2002 while Pax7 knockout mice exhibit craniofacial defects (Hill et al, 1996;Mansouri et al, 1996b). Although hypomorphic mutant studies are beginning to elucidate a mode of action for Pax genes, earlier studies of Pax mutant animals were to some extent hindered by compensation through gene expression of other Pax family members, and, did not, we believe, fully characterize the role of individual Pax genes (Relaix et al, 2004;Zhou et al, 2008).…”