PUBLICATION

A neural degeneration mutation that spares primary neurons in the zebrafish

Authors
Grunwald, D.J., Kimmel, C.B., Westerfield, M., Walker, C., and Streisinger, G.
ID
ZDB-PUB-961014-377
Date
1988
Source
Developmental Biology   126: 115-128 (Journal)
Registered Authors
Grunwald, David, Kimmel, Charles B., Streisinger, George, Walker, Charline, Westerfield, Monte
Keywords
none
MeSH Terms
  • Animals
  • Brain/cytology
  • Brain/embryology*
  • Cell Survival
  • Cyprinidae/genetics*
  • Female
  • Interneurons/physiology
  • Male
  • Motor Neurons/physiology
  • Movement
  • Muscles/physiopathology
  • Mutation*
  • Nerve Degeneration
  • Neuromuscular Junction/physiopathology
  • Neurons/physiology*
  • Neurons, Afferent/physiology
  • Phenotype
  • Spinal Cord/cytology
  • Spinal Cord/embryology*
  • Zebrafish/embryology
  • Zebrafish/genetics*
PubMed
3342929 Full text @ Dev. Biol.
Abstract
We describe an embryonic lethal mutation in the zebrafish Brachydanio rerio that specifically affects the viability of most cells in the embryonic central nervous system (CNS). The mutation ned-1 (b39rl) was induced with gamma-irradiation and segregates as a single recessive allele closely linked to its centromere. It produces massive cell death in the CNS but a small set of specific neurons, including Rohon-Beard sensory neurons, large hindbrain interneurons, and primary motoneurons, survive embryogenesis and are functional. Synaptic connections between embryonic motoneurons and muscle cells appear physiologically normal, and the normally observed spontaneous flexions are present. Correlated with the presence of sensory neurons and interneurons, mutant embryos display reflexive movements in response to mechanical stimulation. Together, the surviving neurons, called primary neurons, form a class of cells that are prominent in size and arise early during development. Thus, this mutation may define a function that is differentially required by developmentally distinguishable sets of cells in the embryonic CNS.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping