Research
Development, Evolution and Disease
Neural crest cells comprise a heterogeneous, multipotent, migratory cell population that generate an astonishing array of cell types and tissues during vertebrate development. This includes cartilage, bone and connective tissues in the head, as well as sensory neurons, glia, smooth muscle and pigment cells amongst many others throughout the body. Neural crest cells have played an integral role in vertebrate evolution, particularly with respect to craniofacial development and organogenesis.
Research in the Trainor laboratory seeks to understand the mechanisms that regulate neural crest cell specification, epithelial to mesenchymal transformation, migration, proliferation, survival and differentiation, and to apply this foundational knowledge to better understand vertebrate development and evolution. However, the same genetic, cellular, and biochemical mechanisms that regulate normal vertebrate development and evolution often go awry in the pathogenesis of birth defects.
1% of all live births exhibit a minor or major developmental anomaly, and those that arise due to defects in neural crest cell development are collectively called neurocristopathies. Craniofacial anomalies account for approximately one-third of all human congenital birth defects and are largely attributed to defects in neural crest cell development. Moreover, depending on which stage of neural crest cell development is disrupted, distinct craniofacial phenotypes can occur. Therefore, understanding the mechanisms that control head and facial development is an important issue. However, the same principle applies not only to neural crest cells and their contributions to craniofacial morphogenesis, but also to peripheral nervous system, cardiac and gastrointestinal development.
Classic models suggested that the genetic identity and lineage fate of neural crest cells were programmed prior to their delamination and migration from the neuroepithelium. However, we demonstrated in mammalian embryos, that neural crest cells are quite plastic and that their development can be influenced by the tissues they interact with during their migration. Thus, congenital neurocristopathies can arise through perturbation of intrinsic and/or extrinsic effects on neural crest cell development.
In the lab, we are particularly interested in craniofacial development and currently study neurocristopathies such as Treacher Collins syndrome, Acrofacial Dysostosis – Cincinnati type, Cleft Lip and Palate, Holoprosencephaly and Syngnathia. However, in addition, we are also investigating the roles of neural crest cells in the pathogenesis of heart and gastrointestinal disorders such as persistent truncus arteriosus and Hirschsprung’s disease respectively. Our long term goal is not only to uncover the etiology and pathogenesis of birth defects, but also to develop therapeutic avenues for their prevention.
Research in the Trainor laboratory seeks to understand the mechanisms that regulate neural crest cell specification, epithelial to mesenchymal transformation, migration, proliferation, survival and differentiation, and to apply this foundational knowledge to better understand vertebrate development and evolution. However, the same genetic, cellular, and biochemical mechanisms that regulate normal vertebrate development and evolution often go awry in the pathogenesis of birth defects.
1% of all live births exhibit a minor or major developmental anomaly, and those that arise due to defects in neural crest cell development are collectively called neurocristopathies. Craniofacial anomalies account for approximately one-third of all human congenital birth defects and are largely attributed to defects in neural crest cell development. Moreover, depending on which stage of neural crest cell development is disrupted, distinct craniofacial phenotypes can occur. Therefore, understanding the mechanisms that control head and facial development is an important issue. However, the same principle applies not only to neural crest cells and their contributions to craniofacial morphogenesis, but also to peripheral nervous system, cardiac and gastrointestinal development.
Classic models suggested that the genetic identity and lineage fate of neural crest cells were programmed prior to their delamination and migration from the neuroepithelium. However, we demonstrated in mammalian embryos, that neural crest cells are quite plastic and that their development can be influenced by the tissues they interact with during their migration. Thus, congenital neurocristopathies can arise through perturbation of intrinsic and/or extrinsic effects on neural crest cell development.
In the lab, we are particularly interested in craniofacial development and currently study neurocristopathies such as Treacher Collins syndrome, Acrofacial Dysostosis – Cincinnati type, Cleft Lip and Palate, Holoprosencephaly and Syngnathia. However, in addition, we are also investigating the roles of neural crest cells in the pathogenesis of heart and gastrointestinal disorders such as persistent truncus arteriosus and Hirschsprung’s disease respectively. Our long term goal is not only to uncover the etiology and pathogenesis of birth defects, but also to develop therapeutic avenues for their prevention.
Paul Trainor, PhD
Investigator, Stowers Institute for Medical Research
Professor, Department of Anatomy & Cell Biology, The University of Kansas School of Medicine
Editor-in-Chief, Developmental Dynamics
Fellow of the American Association of Anatomists
Professor, Department of Anatomy & Cell Biology, The University of Kansas School of Medicine
Editor-in-Chief, Developmental Dynamics
Fellow of the American Association of Anatomists
