Children with Kabuki Syndrome (KS) have neurodevelopment defects that greatly impact the quality of life for KS children and their families. The cellular and molecular mechanisms by which KMT2D mutations cause these neurodevelopmental defects are unknown. We will use the experimental versatility and high-throughput capabilities of our KS zebrafish models and the translatability of KS patient iPSC-derived brain organoids to understand the novel roles of KMT2D during neurogenesis.
