PUBLICATION

The role of Suppressor of Hairless in Notch mediated signalling during zebrafish somitogenesis

Authors
Sieger, D., Tautz, D., and Gajewski, M.
ID
ZDB-PUB-031014-7
Date
2003
Source
Mechanisms of Development   120(9): 1083-1094 (Journal)
Registered Authors
Gajewski, Martin, Sieger, Dirk
Keywords
none
MeSH Terms
  • Intracellular Signaling Peptides and Proteins
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish/metabolism
  • Molecular Sequence Data
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism
  • Somites/metabolism*
  • Animals
  • Cloning, Molecular
  • DNA, Complementary/genetics
  • Receptors, Notch
  • Base Sequence
  • Membrane Proteins/genetics*
  • Membrane Proteins/metabolism
  • Gene Expression Regulation, Developmental
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
  • Gene Targeting
  • Signal Transduction
(all 20)
PubMed
14550536 Full text @ Mech. Dev.
Abstract
Suppressor of Hairless (Su(H)) codes for a protein that interacts with the intracellular domain of Notch to activate the target genes of the Delta-Notch signalling pathway. We have cloned the zebrafish homologue of Su(H) and have analysed its function by morpholino mediated knockdown. While there are at least four notch and four delta homologues in zebrafish, there appears to be only one complete Su(H) homologue. We have analysed the function of Su(H) in the somitogenesis process and its influence on the expression of notch pathway genes, in particular her1, her7, deltaC and deltaD. The cyclic expression of her1, her7 and deltaC in the presomitic mesoderm is disrupted by the Su(H) knockdown mimicking the expression of these genes in the notch1a mutant deadly seven. deltaD expression is similarly affected by Su(H) knockdown like deltaC but shows in addition an ectopic expression in the developing neural tube. The inactivation of Su(H) in a fss/tbx24 mutant background leads furthermore to a clear breakdown of cyclic her1 and her7 expression, indicating that the Delta-Notch pathway is required for the creation of oscillation and not only for the synchronisation between neighbouring cells. The strongest phenotypes in the Su(H) knockdown embryos show a loss of all somites posterior to the first five to seven ones. This phenotype is stronger than the known amorphic phenotypes for notch1 (des) or deltaD (aei) in zebrafish, but mimicks the knockout phenotype of RBP-Jkappa gene in the mouse, which is the homologue of Su(H). This suggests that there is some functional redundancy among the Notch and Delta genes. This fact that the first five to seven somites are only weakly affected by Su(H) knockdown indicates that additional genetic pathways may be active in the specification of the most anterior somites.
Genes / Markers
Figures
No images available
Show all Figures
Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
notch1a_unspecified
    Unspecified
    tbx6_unspecified
      Unspecified
      1 - 2 of 2
      Show
      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      her1MO2-her1MRPHLNO
      rbpjaMO1-rbpjaMRPHLNO
      rbpjaMO4-rbpja,rbpjbMRPHLNO
      rbpjbMO4-rbpja,rbpjbMRPHLNO
      1 - 4 of 4
      Show
      Fish
      1 - 3 of 3
      Show
      Antibodies
      Orthology
      Engineered Foreign Genes
      No data available
      Mapping