In Xenopus laevis several different ISWI complexes have been described, each consisting of a unique combination of protein subunits. Each complex may have its own function during embryonic development and may be expressed at different places or stages in the embryo. Research has shown that knocking down ISWI function in Xenopus embryos leads to misregulation of genes involved in neural patterning and development, such as BMP4 and Sonic Hedgehog (Shh) and that ISWI binds to BMP4 gene in vitro. Partial inhibition of ISWI function results in aberrant eye development and the formation of cataracts. This suggests a critical role for ISWI complexes in neural and eye development. I wish to study the developmental consequences of knocking down ISWI function in specific tissues or at different stages of Xenopus embryos. I am using a dominant negative ISWI mutant, with a point mutation in the ATPase domain which ablates ATPase activity. I am creating transgenic Xenopus embryos in which I have placed this mutant under the control of neural /eye-specific promoters (e.g. gamma crystallin, Otx2, Pax6) in order to understand the role of ISWI in specific developmental pathways.