PUBLICATION

beamter/deltaC and the role of Notch ligands in the zebrafish somite segmentation, hindbrain neurogenesis and hypochord differentiation

Authors
Julich, D., Hwee, Lim C., Round, J., Nicolaije, C., Schroeder, J., Davies, A., Geisler, R., Lewis, J., Jiang, Y.J., Holley, S.A., Tübingen 2000 Screen Consortium.
ID
ZDB-PUB-050831-9
Date
2005
Source
Developmental Biology   286(2): 391-404 (Journal)
Registered Authors
Geisler, Robert, Holley, Scott, Jiang, Yun-Jin, Jülich, Dörthe, Lewis, Julian, Lim, Chiaw Hwee
Keywords
Zebrafish, Somite, Notch, After eight, DeltaD, Beamter, DeltaC, Oscillator
MeSH Terms
  • Animals
  • RNA, Messenger/analysis
  • Gene Expression Regulation, Developmental
  • Alleles
  • Ligands
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins/genetics*
  • Membrane Proteins/physiology
  • Zebrafish/embryology*
  • Biological Clocks/physiology
  • Mutation
  • Receptors, Notch/metabolism
  • Somites*
  • Rhombencephalon/cytology
  • Rhombencephalon/embryology*
  • Rhombencephalon/growth & development
(all 16)
PubMed
16125692 Full text @ Dev. Biol.
Abstract
The Tubingen large-scale zebrafish genetic screen completed in 1996 identified a set of five genes required for orderly somite segmentation. Four of them have been molecularly identified and three were found to code for components of the Notch pathway, which are required for the coordinated oscillation of gene expression, known as the segmentation clock, in the presomitic mesoderm (PSM). Here, we show that the final member of the group, beamter (bea), codes for the Notch ligand DeltaC, and we present and characterize two new alleles, including one allele encoding for a protein truncated in the 7th EGF repeat and an allele deleting only the DSL domain which was previously shown to be necessary for ligand function. Interestingly however, when we over-express any of the mutant deltaC mRNAs, we observe antimorphic effects on both hindbrain neurogenesis and hypochord formation. Expression of bea/deltaC oscillates in the PSM, and a triple fluorescent in situ analysis of its oscillation in relation to that of other oscillating genes in the PSM reveals differences in subcellular localization of the oscillating mRNAs in individual cells in different oscillation phases. Mutations in aei/deltaD and bea/deltaC differ in the way they disrupt the oscillating expression of her1 and deltaC. Furthermore, we find that the double mutants have significantly stronger defects in hypochord formation but not in somitogenesis or hindbrain neurogenesis, indicating genetically that the two delta's may function either semi-redundantly or distinctly, depending upon context.
Genes / Markers
Figures
Figure Gallery (5 images)
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Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
tg249
    Point Mutation
    thf102
      Small Deletion
      tit446
        Point Mutation
        tm98
          Point Mutation
          to202
            Point Mutation
            tr233
              Point Mutation
              tw212b
                Point Mutation
                1 - 7 of 7
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                Human Disease / Model
                No data available
                Sequence Targeting Reagents
                No data available
                Fish
                Antibodies
                No data available
                Orthology
                No data available
                Engineered Foreign Genes
                No data available
                Mapping
                Entity Type Entity Symbol Location
                Featuretm98Chr: 15 Details
                SSLPz7871Chr: 15 Details
                SSLPz8991Chr: 15 Details
                1 - 3 of 3
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