![Exploring Embryonic Development]()
The p53 tumor suppressor gene arrests cell growth and induces cell death, This makes increased p53 expression incompatible with processes involving active growth, such as an embryo’s formation and development. In the August 8 online edition of Nature Communications, Nicholas Sibinga, M.D., and colleagues report that β-catenin—a protein known to have critical functions in embryogenesis and adult homeostasis—plays a key role in regulating p53 during artery formation in embryos. The researchers selectively inactivated β-catenin in smooth muscle cells (SMCs) that surround developing embryonic arteries. They found an absolute requirement for SMC β-catenin in forming arteries in mouse embryos. Loss of β-catenin signaling in SMCs led to impaired artery growth and reduced survival. β-catenin was found to perform its essential role in artery formation in part by inhibiting p53 activity. The study’s lead author was Dario Riascos-Bernal, a recent graduate from the Sibinga lab. Dr. Sibinga is professor of medicine and of developmental and molecular biology.
Posted on: Wednesday, September 07, 2016