Zebrafish deadly seven functions in neurogenesis.

Academic Article


  • In a genetic screen, we isolated a mutation that perturbed motor axon outgrowth, neurogenesis, and somitogenesis. Complementation tests revealed that this mutation is an allele of deadly seven (des). By creating genetic mosaics, we demonstrate that the motor axon defect is non-cell autonomous. In addition, we show that the pattern of migration for some neural crest cell populations is aberrant and crest-derived dorsal root ganglion neurons are misplaced. Furthermore, our analysis reveals that des mutant embryos exhibit a neurogenic phenotype. We find an increase in the number of primary motoneurons and in the number of three hindbrain reticulospinal neurons: Mauthner cells, RoL2 cells, and MiD3cm cells. We also find that the number of Rohon-Beard sensory neurons is decreased whereas neural crest-derived dorsal root ganglion neurons are increased in number supporting a previous hypothesis that Rohon-Beard neurons and neural crest form an equivalence group during development. Mutations in genes involved in Notch-Delta signaling result in defects in somitogenesis and neurogenesis. We found that overexpressing an activated form of Notch decreased the number of Mauthner cells in des mutants indicating that des functions via the Notch-Delta signaling pathway to control the production of specific cell types within the central and peripheral nervous systems.
  • Authors

    Published In


  • Alleles, Animals, Antibodies, Monoclonal, Bromodeoxyuridine, Gene Expression Regulation, Developmental, Genetic Complementation Test, Homeodomain Proteins, Immunohistochemistry, In Situ Hybridization, Membrane Proteins, Mutation, Nerve Tissue Proteins, Nervous System, Neural Crest, Neurons, Phenotype, Plasmids, RNA, Receptor, Notch1, Receptors, Notch, Signal Transduction, Somites, Time Factors, Xenopus, Zebrafish, Zebrafish Proteins
  • Digital Object Identifier (doi)

    Author List

  • Gray M; Moens CB; Amacher SL; Eisen JS; Beattie CE
  • Start Page

  • 306
  • End Page

  • 323
  • Volume

  • 237
  • Issue

  • 2