PUBLICATION

fused-somites-like mutants exhibit defects in trunk vessel patterning

Authors
Shaw, K.M., Castranova, D.A., Pham, V.N., Kamei, M., Kidd, K.R., Lo, B.D., Torres-Vazquez, J., Ruby, A., and Weinstein, B.M.
ID
ZDB-PUB-060412-22
Date
2006
Source
Developmental dynamics : an official publication of the American Association of Anatomists   235(7): 1753-1760 (Journal)
Registered Authors
Castranova, Dan, Kamei, Makoto, Kidd, Kameha, Pham, Van, Torres-Vazquez, Jesus, Weinstein, Brant M.
Keywords
blood vessels, zebrafish, fused somites, beamter, deltaC
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Blood Vessels/embryology*
  • Body Patterning
  • Embryo, Nonmammalian
  • Mutation
  • Neovascularization, Physiologic/genetics
  • Neovascularization, Physiologic/physiology*
  • Nerve Growth Factors/genetics
  • Nerve Growth Factors/metabolism
  • Semaphorins/genetics
  • Semaphorins/metabolism
  • Somites/cytology*
  • Somites/metabolism
  • T-Box Domain Proteins/genetics
  • T-Box Domain Proteins/metabolism
  • Zebrafish
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed
16607654 Full text @ Dev. Dyn.
Abstract
We identified four mutants in two distinct loci exhibiting similar trunk vascular patterning defects in an F3 genetic screen for zebrafish vascular mutants. Initial vasculogenesis is not affected in these mutants, with proper specification and differentiation of endothelial cells. However, all four display severe defects in the growth and patterning of angiogenic vessels in the trunk, with ectopic branching and disoriented migration of intersegmental vessels. The four mutants are allelic to previously characterized mutants at the fused-somites (fss) and beamter (bea) loci, and they exhibit comparable defects in trunk somite boundary formation. The fss locus has been shown to correspond to tbx24; we show here that bea mutants are defective in the zebrafish dlC gene. Somitic expression of known vascular guidance factors efnb2a, sema3a1, and sema3a2 is aberrantly patterned in fss and bea mutants, suggesting that the vascular phenotype is due to loss of proper guidance cues provided by these factors.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes