Normal neural development depends on the precise regulation of spatial and temporal patterns of gene expression during embryogenesis, from early signaling that specifies neural tissues through late induction and differentiation events controlling the final complex structure of the eye and brain. All of this carefully orchestrated transcription must be regulated in the context of chromatin, the complex of DNA and histones that compacts DNA into the eukaryotic nucleus. Chromatin remodeling enzymes and histone modifying enzymes cooperatively regulate the accessibility of DNA in chromatin, and are thereby essential regulators of gene expression. The Imitation Switch (ISWI) chromatin remodeling enzyme is critical for development of the central nervous system and eye in Xenopus laevis. ISWI is present in several different complexes, including the WICH complex, a heterodimer of ISWI and WSTF (Williams Syndrome Transcription Factor). Microdeletion of a set of genes including WSTF results in Williams Syndrome (WS), a neurodevelopmental disorder characterized by a unique spectrum of anomalies including cognitive deficits and visiospacial impairment. WS patients also exhibit characteristic behavior patterns such as hypersociability and a tendency to approach strangers, and WS has become an exciting model for studying the relationship between neural development and behavior. I am studying the specific roles of WSTF in Xenopus development, especially in the development of the brain and eye. The goal of this work is to understand how WICH-dependent chromatin remodeling regulates the transcriptional cascade required for normal neural development and differentiation. In addition to revealing fundamental mechanisms of development of the vertebrate brain and eye, this work can provide new insights into how reduced WSTF may contribute to the complex physical and behavioral abnormalities in Williams Syndrome patients.