PUBLICATION

parachute/n-cadherin is required for morphogenesis and maintained integrity of the zebrafish neural tube

Authors
Lele, Z., Folchert, A., Concha, M., Rauch, G.-J., Geisler, R., Rosa, F., Wilson, S.W., Hammerschmidt, M., and Bally-Cuif, L.
ID
ZDB-PUB-020716-24
Date
2002
Source
Development (Cambridge, England)   129(14): 3281-3294 (Journal)
Registered Authors
Bally-Cuif, Laure, Concha, Miguel, Folchert, Anja, Geisler, Robert, Hammerschmidt, Matthias, Lele, Zsolt, Rauch, Gerd-Jörg, Rosa, Frederic, Wilson, Steve
Keywords
zebrafish; neural tube; parachute; n-cadherin
MeSH Terms
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish Proteins
  • beta Catenin
  • Mutation
  • Cloning, Molecular
  • Rhombencephalon/embryology
  • Cadherins/genetics
  • Cadherins/physiology*
  • Animals
  • Base Sequence
  • Central Nervous System/anatomy & histology
  • Central Nervous System/embryology*
  • Phenotype
  • Cytoskeletal Proteins/metabolism
  • DNA, Complementary/genetics
  • Morphogenesis/genetics
  • Alleles
  • Cell Adhesion/genetics
  • Trans-Activators/metabolism
  • Mesencephalon/embryology
  • Mitosis
(all 23)
PubMed
12091300 Full text @ Development
Abstract
N-cadherin (Ncad) is a classical cadherin that is implicated in several aspects of vertebrate embryonic development, including somitogenesis, heart morphogenesis, neural tube formation and establishment of left-right asymmetry. However, genetic in vivo analyses of its role during neural development have been rather limited. We report the isolation and characterization of the zebrafish parachute (pac) mutations. By mapping and candidate gene analysis, we demonstrate that pac corresponds to a zebrafish n-cadherin (ncad) homolog. Three mutant alleles were sequenced and each is likely to encode a non-functional Ncad protein. All result in a similar neural tube phenotype that is most prominent in the midbrain, hindbrain and the posterior spinal cord. Neuroectodermal cell adhesion is altered, and convergent cell movements during neurulation are severely compromised. In addition, many neurons become progressively displaced along the dorsoventral and the anteroposterior axes. At the cellular level, loss of Ncad affects beta-catenin stabilization/localization and causes mispositioned and increased mitoses in the dorsal midbrain and hindbrain, a phenotype later correlated with enhanced apoptosis and the appearance of ectopic neurons in these areas. Our results thus highlight novel and crucial in vivo roles for Ncad in the control of cell convergence, maintenance of neuronal positioning and dorsal cell proliferation during vertebrate neural tube development.
Genes / Markers
Figures
Figure Gallery (7 images)
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
fr7
    Point Mutation
    r210
      Point Mutation
      tc248c
        Unknown
        tg1a
          Unknown
          tg299b
            Unknown
            tj250a
              Unknown
              tm101
                Point Mutation
                1 - 7 of 7
                Show
                Human Disease / Model
                No data available
                Sequence Targeting Reagents
                Target Reagent Reagent Type
                cdh2MO1-cdh2MRPHLNO
                cdh2MO2-cdh2MRPHLNO
                1 - 2 of 2
                Show
                Fish
                Antibodies
                No data available
                Orthology
                No data available
                Engineered Foreign Genes
                No data available
                Mapping
                Entity Type Entity Symbol Location
                GENEcdh2Chr: 20 Details
                SSLPz3964Chr: 20 Details
                1 - 2 of 2
                Show