Notch pathway regulation of neural crest cell development in vivo.

The Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.

Developmental dynamics : an official publication of the American Association of Anatomists 2012 Feb

filter terms:

The function of Notch signaling in murine neural crest-derived cell lineages in vivo was examined. Conditional gain (Wnt1Cre;Rosa(Notch)) or loss (Wnt1Cre;RBP-J(f/f)) of Notch signaling in neural crest cells (NCCs) in vivo results in craniofacial, cardiac, and trunk abnormalities. Severe craniofacial malformations are apparent in Wnt1Cre;Rosa(Notch) embryos, while less severe skull abnormalities are evident in Wnt1Cre;RBP-J(f/f) mice. Deficient cardiac neural crest migration, resulting in cardiac outflow tract malformations, occurs with increased or decreased Notch signaling in NCCs. Smooth muscle cell differentiation also is impaired in pharyngeal NCC derivatives in both Wnt1Cre;Rosa(Notch) and Wnt1Cre;RBP-J(f/f) embryos. Neurogenesis is absent and gliogenesis is increased in the dorsal root ganglia of Wnt1Cre;Rosa(Notch) embryos, while neurogenesis is increased and gliogenesis is decreased in Wnt1Cre;RBP-J(f/f) embryos. Together, these studies demonstrate essential cell-autonomous roles for appropriate levels of Notch signaling during NCC migration, proliferation, and differentiation with critical implications in craniofacial, cardiac, and neurogenic development and disease. Copyright © 2012 Wiley-Liss, Inc.

Citation

Timothy J Mead, Katherine E Yutzey. Notch pathway regulation of neural crest cell development in vivo. Developmental dynamics : an official publication of the American Association of Anatomists. 2012 Feb;241(2):376-89