PUBLICATION
A role for chemokine signaling in neural crest cell migration and craniofacial development
- Authors
- Olesnicky Killian, E.C., Birkholz, D.A., and Artinger, K.B.
- ID
- ZDB-PUB-090714-2
- Date
- 2009
- Source
- Developmental Biology 333(1): 161-172 (Journal)
- Registered Authors
- Artinger, Kristin Bruk
- Keywords
- chemokine, cxcr4, sdf1, cxcr7, neural crest, migration, neurocranium, endoderm
- MeSH Terms
-
- Animals
- Body Patterning/physiology
- Branchial Region/embryology
- Branchial Region/metabolism
- Cartilage/embryology
- Cartilage/metabolism
- Cell Differentiation/physiology
- Cell Movement/physiology
- Chemokine CXCL12/metabolism*
- Embryo, Nonmammalian
- Endoderm/embryology
- Endoderm/metabolism
- Neural Crest/embryology
- Neural Crest/physiology*
- Receptors, CXCR/metabolism*
- Receptors, CXCR4/metabolism*
- Signal Transduction
- Skull/embryology*
- Skull/metabolism
- Zebrafish
- Zebrafish Proteins/metabolism*
- PubMed
- 19576198 Full text @ Dev. Biol.
Citation
Olesnicky Killian, E.C., Birkholz, D.A., and Artinger, K.B. (2009) A role for chemokine signaling in neural crest cell migration and craniofacial development. Developmental Biology. 333(1):161-172.
Abstract
Neural crest cells (NCCs) are a unique population of multipotent cells that migrate along defined pathways throughout the embryo and give rise to many diverse cell types including pigment cells, craniofacial cartilage and the peripheral nervous system (PNS). Aberrant migration of NCCs results in a wide variety of congenital birth defects including craniofacial abnormalities. The chemokine Sdf1 and its receptors, Cxcr4 and Cxcr7, have been identified as key components in the regulation of cell migration in a variety of tissues. Here we describe a novel role for the zebrafish chemokine receptor Cxcr4a in the development and migration of cranial NCCs (CNCCs). We find that loss of Cxcr4a, but not Cxcr7b results in aberrant CNCC migration, defects in the neurocranium, as well as cranial ganglia dismorphogenesis. Moreover, overexpression of either Sdf1b or Cxcr4a causes aberrant CNCC migration and results in ectopic craniofacial cartilages. We propose a model in which Sdf1b signaling from the pharyngeal arch endoderm and optic stalk to Cxcr4a expressing CNCCs is important for both the proper condensation of the CNCCs into pharyngeal arches and the subsequent patterning and morphogenesis of the neural crest derived tissues.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping