ZFIN ID: ZDB-PUB-050413-3
Integrinalpha5 and Delta/Notch Signaling Have Complementary Spatiotemporal Requirements during Zebrafish Somitogenesis
Jülich, D., Geisler, R., Tübingen 2000 Screen Consortium, and Holley, S.A.
Date: 2005
Source: Developmental Cell   8(4): 575-586 (Journal)
Registered Authors: Geisler, Robert, Holley, Scott, Jülich, Dörthe
Keywords: none
MeSH Terms:
  • Amino Acid Sequence
  • Animals
  • Animals, Genetically Modified
  • Body Patterning*
  • Cell Polarity
  • Extracellular Matrix/chemistry
  • Extracellular Matrix/metabolism
  • Fibronectins/metabolism
  • Gene Expression Regulation, Developmental
  • In Situ Hybridization
  • Integrin alpha5/genetics
  • Integrin alpha5/metabolism*
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins/genetics
  • Membrane Proteins/metabolism*
  • Molecular Sequence Data
  • Morphogenesis
  • Phenotype
  • Point Mutation
  • Receptors, Notch
  • Recombinant Fusion Proteins/genetics
  • Recombinant Fusion Proteins/metabolism
  • Signal Transduction/physiology*
  • Somites/cytology
  • Somites/physiology*
  • Zebrafish/anatomy & histology
  • Zebrafish/embryology*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 15809039 Full text @ Dev. Cell
Somitogenesis is the process by which the segmented precursors of the skeletal muscle and vertebral column are generated during vertebrate embryogenesis. While somitogenesis appears to be a serially homologous, reiterative process, we find that there are differences between the genetic control of early/anterior and late/posterior somitogenesis. We demonstrate that point mutations can cause segmentation defects in either the anterior, middle, or posterior somites in the zebrafish. We find that mutations in zebrafish integrinalpha5 disrupt anterior somite formation, giving a phenotype complementary to the posterior defects seen in the notch pathway mutants after eight/deltaD and deadly seven/notch1a. Double mutants between the notch pathway and integrinalpha5 display somite defects along the entire body axis, with a complete loss of the mesenchymal-to-epithelial transition and Fibronectin matrix assembly in the posterior. Our data suggest that notch- and integrinalpha5-dependent cell polarization and Fibronectin matrix assembly occur concomitantly and interdependently during border morphogenesis.