PUBLICATION
Zebrafish notch signalling pathway mutants exhibit trunk vessel patterning anomalies that are secondary to somite misregulation
- Authors
- Therapontos, C., and Vargesson, N.
- ID
- ZDB-PUB-101108-12
- Date
- 2010
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 239(10): 2761-2768 (Journal)
- Registered Authors
- Keywords
- after-eight, beamter, deadly-seven, angiogenesis, filopodia, somites, intersomitic vessels, dll4
- MeSH Terms
-
- Animals
- Body Patterning/genetics
- Body Patterning/physiology*
- Gene Expression Regulation, Developmental/genetics
- Gene Expression Regulation, Developmental/physiology
- Immunohistochemistry
- In Situ Hybridization
- Nerve Growth Factors/genetics
- Nerve Growth Factors/metabolism
- Receptors, Cell Surface/genetics
- Receptors, Cell Surface/metabolism
- Receptors, Notch/genetics
- Receptors, Notch/metabolism*
- Reverse Transcriptase Polymerase Chain Reaction
- Signal Transduction/genetics
- Signal Transduction/physiology
- Somites/embryology*
- Somites/metabolism*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 21038448 Full text @ Dev. Dyn.
Citation
Therapontos, C., and Vargesson, N. (2010) Zebrafish notch signalling pathway mutants exhibit trunk vessel patterning anomalies that are secondary to somite misregulation. Developmental Dynamics : an official publication of the American Association of Anatomists. 239(10):2761-2768.
Abstract
The Notch signalling pathway mutants, after-eight (aei), beamter (bea), and deadly-seven (des) have previously been used to study somitogenesis and neurogenesis. Notch signalling has also been shown to have roles in vascular development. However, vascular development in each of these three Notch mutants has not been described, and so their potential usefulness for further understanding the role of Notch signalling in angiogenesis is unknown. Here we demonstrate each of the mutants also exhibit vascular defects in inter-somitic vessel (ISV) positioning and patterning. Ectopic filopodia were also observed on the ISVs of the mutants. Ectopic filopodia are not due to loss of dll4. Somite expression of known vascular guidance cues, efnb2, sema3a2, and plexinD1 are disrupted, suggesting that the ISV vascular phenotype is due to disruption of these cues.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping