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Dev Biol. 2014 May 1;389(1):39-49. doi: 10.1016/j.ydbio.2013.11.025. Epub 2013 Dec 3.

Signaling mechanisms controlling cranial placode neurogenesis and delamination.

Author information

1
Institute for Pediatric Regenerative Medicine at Shriners Hospitals for Children-Northern California, CA 95817, USA; Department of Cell Biology and Human Anatomy, University of California Davis, School of Medicine, Sacramento, CA 95817, USA. Electronic address: rlassiter@saddleback.edu.
2
Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA. Electronic address: michael_stark@byu.edu.
3
Institute for Pediatric Regenerative Medicine at Shriners Hospitals for Children-Northern California, CA 95817, USA; Department of Cell Biology and Human Anatomy, University of California Davis, School of Medicine, Sacramento, CA 95817, USA.
4
Institute for Pediatric Regenerative Medicine at Shriners Hospitals for Children-Northern California, CA 95817, USA; Department of Cell Biology and Human Anatomy, University of California Davis, School of Medicine, Sacramento, CA 95817, USA; Department of Biochemistry and Molecular Medicine, University of California Davis, School of Medicine, Sacramento, CA 95817, USA. Electronic address: cjzhou@ucdavis.edu.

Abstract

The neurogenic cranial placodes are a unique transient epithelial niche of neural progenitor cells that give rise to multiple derivatives of the peripheral nervous system, particularly, the sensory neurons. Placode neurogenesis occurs throughout an extended period of time with epithelial cells continually recruited as neural progenitor cells. Sensory neuron development in the trigeminal, epibranchial, otic, and olfactory placodes coincides with detachment of these neuroblasts from the encompassing epithelial sheet, leading to delamination and ingression into the mesenchyme where they continue to differentiate as neurons. Multiple signaling pathways are known to direct placodal development. This review defines the signaling pathways working at the finite spatiotemporal period when neuronal selection within the placodes occurs, and neuroblasts concomitantly delaminate from the epithelium. Examining neurogenesis and delamination after initial placodal patterning and specification has revealed a common trend throughout the neurogenic placodes, which suggests that both activated FGF and attenuated Notch signaling activities are required for neurogenesis and changes in epithelial cell adhesion leading to delamination. We also address the varying roles of other pathways such as the Wnt and BMP signaling families during sensory neurogenesis and neuroblast delamination in the differing placodes.

KEYWORDS:

BMP; Cranial placodes; Delamination; FGF; Neurogenesis; Notch; Wnt

PMID:
24315854
PMCID:
PMC3972360
DOI:
10.1016/j.ydbio.2013.11.025
[Indexed for MEDLINE]
Free PMC Article

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