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ZFIN ID: ZDB-PUB-040427-2
Cadherin-2 function in the cranial ganglia and lateral line system of developing zebrafish
Kerstetter, A.E., Azodi, E., Marrs, J.A., and Liu, Q.
Date: 2004
Source: Developmental dynamics : an official publication of the American Association of Anatomists   230(1): 137-143 (Journal)
Registered Authors: Liu, Qin, Marrs, James A.
Keywords: zebrafish, development, neuromasts, cell adhesion molecules, cranial nerves
MeSH Terms:
  • Animals
  • Basal Ganglia/embryology
  • Brain/embryology
  • Cadherins/biosynthesis
  • Cell Adhesion
  • Cell Adhesion Molecules/biosynthesis*
  • Cell Membrane/metabolism
  • Gene Expression Regulation, Developmental*
  • Immunohistochemistry
  • In Situ Hybridization
  • Models, Anatomic
  • Neurons/metabolism
  • Oligonucleotides, Antisense/metabolism
  • Zebrafish
  • Zebrafish Proteins/chemistry
PubMed: 15108318 Full text @ Dev. Dyn.
Cadherins are cell surface molecules that mediate cell-cell adhesion through homophilic interactions. Cadherin-2 (also called N-cadherin), a member of classic cadherin subfamily, has been shown to play important roles in development of a variety of tissues and organs, including the nervous system. We recently reported that cadherin-2 was strongly expressed by the majority of cranial ganglia and lateral line system of developing zebrafish. To gain insight into cadherin-2 role in the formation of these structures, we have used several markers to analyze zebrafish embryos injected with a specific cadherin-2 antisense morpholino oligonucleotide (cdh2MO). We find that development of several cranial ganglia, including the trigeminal, facial, and vagal ganglia, and the lateral line ganglia and neuromasts of the cdh2MO-injected embryos are severely disrupted. These phenotypes were confirmed by analyzing a cadherin-2 mutant, glass onion. Our results suggest that cadherin-2 function is crucial for the normal formation of the zebrafish lateral line system and a subset of cranial ganglia. Developmental Dynamics 230:137-143, 2004. Copyright 2004 Wiley-Liss, Inc.