ZFIN ID: ZDB-PUB-961014-580
Genetic control of primary neuronal development in zebrafish
Kimmel, C.B., Hatta, K., and Eisen, J.S.
Date: 1991
Source: Development (Cambridge, England)   (Suppl.) 2: 47-57 (Review)
Registered Authors: Eisen, Judith S., Hatta, Kohei, Kimmel, Charles B.
Keywords: genetics, mutation, zebrafish, primary neuron, notoneuron, somite, muscle, notochord, floor plate, cell nteractions
MeSH Terms:
  • Animals
  • Embryonic Induction/genetics*
  • Genes, Lethal/physiology
  • Motor Neurons/physiology*
  • Muscles/embryology*
  • Mutagenesis
  • Nervous System/embryology*
  • Neurons/physiology
  • Phenotype
  • Spinal Cord/embryology
  • Synapses/physiology*
  • Zebrafish
PubMed: 1842357
During the first day of embryogenesis in the zebrafish, a precise and relatively simple network of neurons develops, pioneering axonal pathways and apparently functioning to mediate reflexive motor responses to touch stimuli. We have begun to use zygotic lethal mutations to analyze the assembly of this 'primary' embryonic nervous system. Here we focus on spinal primary motoneurons, their inputs from hindbrain Mauthner neurons, and their outputs to segmental body wall muscle. The mutation nic-1 blocks synaptic transmission between nerve and muscle, yet embryonic primary motoneurons appear normal, suggesting that functional interactions with their targets are not involved in regulating their development. The mutation spt-1 directly disrupts development of this muscle, and the mutation cyc-1 appears to directly block specification of the floor plate. Both spt-1 and cyc-1 affect aspects of primary neuronal development, and they probably do so indirectly. The nonautonomous actions of these mutations are local and they produce variable neuronal phenotypes. The observations can be interpreted to mean that some cellular interactions that specify the neurons and their axonal paths occur at close range and involve multiple, possibly combinatorial, transmitter-independent pathways.