PUBLICATION

Semaphorin signaling guides cranial neural crest cell migration in zebrafish

Authors
Yu, H.H., and Moens, C.B.
ID
ZDB-PUB-050513-3
Date
2005
Source
Developmental Biology   280(2): 373-385 (Journal)
Registered Authors
Moens, Cecilia, Yu, Hung-Hsiang (Sam)
Keywords
Cranial neural crest migration; Pbx; Neuropilin; Semaphorin
MeSH Terms
  • Animals
  • Cell Lineage
  • Cell Movement
  • Gene Expression Regulation, Developmental*
  • In Situ Hybridization
  • Ligands
  • Membrane Proteins/metabolism
  • Mosaicism
  • Mutation
  • Nerve Tissue Proteins/metabolism
  • Neural Crest/cytology*
  • Neuropilins/metabolism
  • Phenotype
  • RNA, Messenger/metabolism
  • Semaphorins/metabolism*
  • Signal Transduction
  • Zebrafish
PubMed
15882579 Full text @ Dev. Biol.
Abstract
Cranial neural crest cells (NCCs) migrate into the pharyngeal arches in three primary streams separated by two cranial neural crest (NC)-free zones. Multiple tissues have been implicated in the guidance of cranial NCC migration; however, the signals provided by these tissues have remained elusive. We investigate the function of semaphorins (semas) and their receptors, neuropilins (nrps), in cranial NCC migration in zebrafish. We find that genes of the sema3F and sema3G class are expressed in the cranial NC-free zones, while nrp2a and nrp2b are expressed in the migrating NCCs. sema3F/3G expression is expanded homogeneously in the head periphery through which the cranial NCCs migrate in lzr/pbx4 mutants, in which the cranial NC streams are fused. Antisense morpholino knockdown of Sema3F/3G or Nrp2 suppresses the abnormal cranial NC phenotype of lzr/pbx4 mutants, demonstrating that aberrant Sema3F/3G-Nrp2 signaling is responsible for this phenotype and suggesting that repulsive Sema3F/3G-Npn2 signaling normally contributes to the guidance of migrating cranial NCCs. Furthermore, global over-expression of sema3Gb phenocopies the aberrant cranial NC phenotype of lzr/pbx4 mutants when endogenous Sema3 ligands are knocked down, consistent with a model in which the patterned expression of Sema3 ligands in the head periphery coordinates the migration of Nrp-expressing cranial NCCs.
Genes / Markers
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping