PUBLICATION

Zebrafish semaphorin Z1b inhibits growing motor axons in vivo

Authors
Roos, M., Schachner, M., and Bernhardt, R.R.
ID
ZDB-PUB-991020-5
Date
1999
Source
Mechanisms of Development   87(1-2): 103-117 (Journal)
Registered Authors
Bernhardt, Robert, Roos, Marc, Schachner, Melitta
Keywords
embryo; somites; rhombomeres; recognition molecules; collapsin; semaphorin; axon guidance; repulsion; motor axon; overexpression
MeSH Terms
  • Blotting, Western
  • Cloning, Molecular
  • Mutagenesis
  • Zebrafish Proteins
  • Nerve Growth Factors/genetics
  • Nerve Growth Factors/metabolism*
  • Nerve Growth Factors/physiology*
  • DNA, Complementary/metabolism
  • Somites/metabolism
  • Animals
  • Sequence Homology, Amino Acid
  • Amino Acid Sequence
  • Zebrafish
  • RNA, Messenger/metabolism
  • Time Factors
  • Motor Neurons/cytology
  • Motor Neurons/metabolism
  • Gene Expression Regulation, Developmental*
  • Axons/physiology
  • Molecular Sequence Data
  • Protein Biosynthesis
  • In Situ Hybridization
PubMed
10495275 Full text @ Mech. Dev.
Abstract
Zebrafish semaphorin 1b (sema Z1b) is a new member of the semaphorin family, related to mammalian sema D/III. It is expressed in rhombomeres three and five, and in the posterior half of newly formed somites which is avoided by ventrally extending motor axons. Embryos injected at the 1-2 cell stage with synthetic sema Z1b mRNA developed normally but many (63%) showed missing or severely stunted ventral motor nerves. Other axons, somites, and hindbrain rhombomeres were not affected. No abnormalities were seen in control embryos injected with lacZ mRNA. Sema Z1b might normally influence the midsegmental pathway choice of the ventrally extending motor axons by contributing to a repulsive domain in the posterior somite.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping