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

Dev Dyn. 2006 Jul;235(7):1753-60. doi: 10.1002/dvdy.20814.

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.

Publication types

  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't

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

Substances

  • Nerve Growth Factors
  • Semaphorins
  • T-Box Domain Proteins
  • Zebrafish Proteins
  • sema3aa protein, zebrafish
  • sema3ab protein, zebrafish
  • tbx6 protein, zebrafish