PUBLICATION
Integrinalpha5 and Delta/Notch Signaling Have Complementary Spatiotemporal Requirements during Zebrafish Somitogenesis
- Authors
- Jülich, D., Geisler, R., Tübingen 2000 Screen Consortium, and Holley, S.A.
- ID
- ZDB-PUB-050413-3
- Date
- 2005
- Source
- Developmental Cell 8(4): 575-586 (Journal)
- Registered Authors
- Geisler, Robert, Holley, Scott, Jülich, Dörthe
- Keywords
- none
- MeSH Terms
-
- Intracellular Signaling Peptides and Proteins
- Animals
- Zebrafish/anatomy & histology
- Zebrafish/embryology*
- Zebrafish/physiology
- Amino Acid Sequence
- Somites/cytology
- Somites/physiology*
- Point Mutation
- Gene Expression Regulation, Developmental
- Morphogenesis
- Recombinant Fusion Proteins/genetics
- Recombinant Fusion Proteins/metabolism
- Molecular Sequence Data
- Body Patterning*
- Extracellular Matrix/chemistry
- Extracellular Matrix/metabolism
- Phenotype
- In Situ Hybridization
- Integrin alpha5/genetics
- Integrin alpha5/metabolism*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- Animals, Genetically Modified
- Membrane Proteins/genetics
- Membrane Proteins/metabolism*
- Signal Transduction/physiology*
- Receptors, Notch
- Cell Polarity
- Fibronectins/metabolism
- PubMed
- 15809039 Full text @ Dev. Cell
Citation
Jülich, D., Geisler, R., Tübingen 2000 Screen Consortium, and Holley, S.A. (2005) Integrinalpha5 and Delta/Notch Signaling Have Complementary Spatiotemporal Requirements during Zebrafish Somitogenesis. Developmental Cell. 8(4):575-586.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping