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ZIRC
ZFIN ID: ZDB-PUB-061227-33
Cadherin-2 participates in the morphogenesis of the zebrafish inner ear
Babb-Clendenon, S., Shen, Y.C., Liu, Q., Turner, K.E., Mills, M.S., Cook, G.W.,Miller, C.A., Gattone, V.H. 2nd, Barald, K.F., and Marrs, J.A.
Date: 2006
Source: Journal of Cell Science 119(24): 5169-5177 (Journal)
Registered Authors: Barald, Kate, Liu, Qin, Marrs, James A., Shen, YuChi
Keywords: N-cadherin, Zebrafish, Ear development, Morphogenesis, Antisense oligonucleotide
MeSH Terms:
  • Animals
  • Cadherins/genetics
  • Cadherins/metabolism
  • Cadherins/physiology*
  • Cell Adhesion/genetics
  • Cell Adhesion/physiology
  • Ear, Inner/cytology
  • Ear, Inner/growth & development
  • Ear, Inner/metabolism*
  • Gene Expression Regulation, Developmental
  • Hair Cells, Auditory/cytology
  • Hair Cells, Auditory/metabolism
  • Hair Cells, Auditory/ultrastructure
  • In Situ Hybridization
  • Microscopy, Electron, Transmission
  • Morphogenesis/genetics
  • Morphogenesis/physiology*
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/physiology
PubMed: 17158919 Full text @ J. Cell Sci.
FIGURES
ABSTRACT
Molecular mechanisms that control inner ear morphogenesis from the placode to the three-dimensional functional organ are not well understood. We hypothesize that cell-cell adhesion, mediated by cadherin molecules, contributes significantly to various stages of inner ear formation. Cadherin-2 (Cdh2) function during otic vesicle morphogenesis was investigated by examining morpholino antisense oligonucleotide knockdown and glass onion (glo) (Cdh2 mutant) zebrafish embryos. Placode formation, vesicle cavitation and specification occurred normally, but morphogenesis of the otic vesicle was affected by Cdh2 deficiency: semicircular canals were reduced or absent. Phalloidin staining of the hair cell stereocillia demonstrated that cadherin-2 (cdh2) loss-of-function did not affect hair cell number, but acetylated tubulin labeling showed that hair cell kinocilia were shorter and irregularly shaped. Statoacoustic ganglion size was significantly reduced, which suggested that neuron differentiation or maturation was affected. Furthermore, cdh2 loss-of-function did not cause a general developmental delay, since differentiation of other tissues, including eye, proceeded normally. These findings demonstrate that Cdh2 selectively affects epithelial morphogenetic cell movements, particularly semicircular canal formation, during normal ear mophogenesis.
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