Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development

Abstract

SummaryDuring vertebrate craniofacial development, neural crest cells (NCCs) contribute much of the cartilage, bone and connective tissue that make up the developing head. Although the initial patterns of NCC segmentation and migration are conserved between species, the variety of vertebrate facial morphologies that exist indicates that a complex interplay occurs between intrinsic genetic NCC programs and extrinsic environmental signals during morphogenesis. Here, we review recent work that has begun to shed light on the molecular mechanisms that govern the spatiotemporal patterning of NCC-derived skeletal structures -advances that are central to understanding craniofacial development and its evolution.

Controlled levels of canonical Wnt signaling are required for neural crest migration

“…Therefore, investigation of NC migration provides a deeper understanding of the molecular machinery govering the progression and invasivnes of metastatic cancer. Once NC cells reach their final location, they differentiate into various cell types including peripheral and enteric neurons, glia, smooth muscle cells, craniofacial cartilage and bone, endocrine cells and pigment cells (Dupin et al, 2006;Grenier et al, 2009;Hall, 2008;Kirby and Hutson, 2010;Le Douarin and Kalcheim, 1999;Le Douarin and Teillet, 1971;Minoux andRijli, 2010 andMayor, 2011a) ( Fig.1.1C). Consequently many different systems like skin, face, and heart will have a contribution from the NC cells.…”

Hand1 phosphoregulation within the distal arch neural crest is essential for craniofacial morphogenesis

“…Neural crest cells (NCCs) are a multipotent cell population that specifies within the dorsal lip of the neural tube and subsequently delaminates, migrates and populates the pharyngeal arches (PAs), before ultimately differentiating into a wide spectrum of structures/ tissues along the anterior-posterior (AP) axis of vertebrate embryos (Clouthier et al, 2010;Minoux and Rijli, 2010;Ruest and Clouthier, 2009;Trainor, 2005;Gitton et al, 2010). The NCCs that migrate into the first and second PAs are primarily responsible for orchestrating craniofacial development.…”

Investigation of orofacial stem cell niches and their innervation through microfluidic devices

“…Although much information on the genes that are important for odontogenesis in humans has been revealed using the mouse model, very little is known on the generation of human dental pathologies. Tooth agenesis is the most frequent developmental malformation within the orofacial complex (Mitsiadis and Luder, 2011; Shimizu and Maeda, 2009). Hypodontia refers to the absence of one to six teeth, oligodontia designates the absence of more than six teeth, and anodontia indicates the absence of all teeth (Shimizu and Maeda, 2009).…”

“…In total, the prevalence of permanent tooth agenesis ranges from 1.6 % to 9.6 % in the general population, excluding third molars (Vastardis, 2000). Most cases of tooth agenesis are non-syndromic since they occur without developmental defects in other organs (Mitsiadis and Luder, 2011). However, tooth agenesis could be also part of syndromes that affect orofacial tissues such as Down syndrome, cleft lip and palate, and ectodermal dysplasias.…”

“…Most cases of tooth agenesis are non-syndromic since they occur without developmental defects in other organs (Mitsiadis and Luder, 2011). However, tooth agenesis could be also part of syndromes that affect orofacial tissues such as Down syndrome, cleft lip and palate, and ectodermal dysplasias.Amelogenesis imperfecta (AI) designates another hereditary developmental malformation that affects the structure and appearance of enamel (Crawford et al, 2007;Mitsiadis and Luder, 2011). In a strict sense, the definition of AI includes only enamel dysplasias, which occur in the absence of defects in other tissues, and can be phenotypically classified into three different types.…”