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ZFIN ID: ZDB-PUB-060412-22
fused-somites-like mutants exhibit defects in trunk vessel patterning
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.
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.
FIGURES
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.
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