Inhibition of Notch signaling rescues cardiovascular development in Kabuki Syndrome Kabuki Syndrome patients have a spectrum of congenital disorders, including congenital heart defects, the primary determinant of mortality. Seventy percent of Kabuki Syndrome patients have mutations in the histone methyl-transferase KMT2D. However, the underlying mechanisms that drive these congenital disorders are unknown. Here, we generated…
Here, we show that neural crest derived cardiomyocytes (NC-Cms) in the zebrafish ventricle express Notch ligand jag2b, are adjacent to Notch responding cells, and persist throughout life. Genetic ablation of NC-Cms during embryogenesis results in diminished jag2b, altered Notch signaling and aberrant trabeculation patterns, but is not detrimental to early heart function or survival to adulthood. However,…
Neurobiology & Anatomy Department News highlights recent Yost lab paper https://medicine.utah.edu/neurobiology-anatomy/news/2018/11/yost-nature-communications-paper.php
Angie Serrano has uploaded her preprint https://www.biorxiv.org/content/10.1101/489757v1 Here we show a regulatory link between Notch pathway and Kmt2d during vasculogenesis. Pharmacological inhibition of Notch signaling rescues cardiovascular phenotype in zebrafish Kabuki Syndrome.