PUBLICATION

DeltaC and DeltaD interact as Notch ligands in the zebrafish segmentation clock

Authors
Wright, G.J., Giudicelli, F., Soza-Ried, C., Hanisch, A., Ariza-McNaughton, L., and Lewis, J.
ID
ZDB-PUB-110613-26
Date
2011
Source
Development (Cambridge, England)   138: 2947-2956 (Journal)
Registered Authors
Lewis, Julian, Wright, Gavin J.
Keywords
notch signalling, deltaC, deltaD, segmentation clock, zebrafish
MeSH Terms
  • Recombinant Proteins/metabolism
  • Membrane Proteins/immunology
  • Membrane Proteins/metabolism*
  • Nervous System/metabolism
  • Antibodies, Monoclonal/metabolism*
  • Image Processing, Computer-Assisted
  • Nerve Tissue Proteins/immunology
  • Nerve Tissue Proteins/metabolism*
  • In Situ Hybridization
  • Microscopy, Confocal
  • Immunoprecipitation
  • Gene Expression Regulation, Developmental/physiology*
  • Mesoderm/metabolism
  • Signal Transduction/physiology*
  • Animals
  • Immunohistochemistry
  • Intracellular Signaling Peptides and Proteins/immunology
  • Intracellular Signaling Peptides and Proteins/metabolism*
  • Zebrafish/embryology*
  • Zebrafish Proteins/immunology
  • Zebrafish Proteins/metabolism*
  • Receptors, Notch/metabolism*
(all 22)
PubMed
21653612 Full text @ Development
Abstract
We describe the production and characterisation of two monoclonal antibodies, zdc2 and zdd2, directed against the zebrafish Notch ligands DeltaC and DeltaD, respectively. We use our antibodies to show that these Delta proteins can bind to one another homo- and heterophilically, and to study the localisation of DeltaC and DeltaD in the zebrafish nervous system and presomitic mesoderm (PSM). Our findings in the nervous system largely confirm expectations from previous studies, but in the PSM we see an unexpected pattern in which the localisation of DeltaD varies according to the level of expression of DeltaC: in the anterior PSM, where DeltaC is plentiful, the two proteins are colocalised in intracellular puncta, but in the posterior PSM, where DeltaC is at a lower level, DeltaD is seen mainly on the cell surface. Forced overexpression of DeltaC reduces the amount of DeltaD on the cell surface in the posterior PSM; conversely, loss-of-function mutation of DeltaC increases the amount of DeltaD on the cell surface in the anterior PSM. These findings suggest an explanation for a long-standing puzzle regarding the functions of the two Delta proteins in the somite segmentation clock - an explanation that is based on the proposition that they associate heterophilically to activate Notch.
Genes / Markers
Figures
Figure Gallery (7 images)
Show all Figures
Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
cj2TgTransgenic Insertion
    ta52b
      		Point Mutation
      tr233
        		Point Mutation
        tw212b
          		Point Mutation
          vu22TgTransgenic Insertion
            1 - 5 of 5
            Show
            Human Disease / Model
            No data available
            Sequence Targeting Reagents
            No data available
            Fish
            Fish
            cj2Tg; vu22Tg
            dlctw212b/tw212b
            dldtr233/tr233
            mib1ta52b/ta52b
            1 - 4 of 4
            Show
            Antibodies
            Name Type Antigen Genes Isotypes Host Organism
            Ab1-dlcmonoclonal
              		Mouse
              Ab1-dldmonoclonalIgG1Mouse
              Ab2-ctnnb1polyclonalRabbit
              Ab2-dlcmonoclonal
                		IgG2aMouse
                1 - 4 of 4
                Show
                Orthology
                No data available
                Engineered Foreign Genes
                Marker Marker Type Name
                GAL4EFGGAL4
                1 - 1 of 1
                Show
                Mapping
                No data available
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                Citation
                Wright, G.J., Giudicelli, F., Soza-Ried, C., Hanisch, A., Ariza-McNaughton, L., and Lewis, J. (2011) DeltaC and DeltaD interact as Notch ligands in the zebrafish segmentation clock. Development (Cambridge, England). 138:2947-2956.