PUBLICATION

Mosaic hoxb4a neuronal pleiotropism in zebrafish caudal hindbrain

Authors
Ma, L.H., Punnamoottil, B., Rinkwitz, S., and Baker, R.
ID
ZDB-PUB-090622-11
Date
2009
Source
PLoS One   4(6): e5944 (Journal)
Registered Authors
Baker, Robert, Ma, Leung-Hang Omicron, Punnamoottil, Beena, Rinkwitz, Silke
Keywords
Neurons, Hindbrain, Yellow fluorescent protein, Neural pathways, Zebrafish, Cerebellum, Spinal cord, Mutant genotypes
MeSH Terms
  • Animals
  • Axons
  • Body Patterning
  • Fluorescent Dyes/pharmacology
  • Gene Expression Regulation
  • Homeodomain Proteins/metabolism*
  • In Situ Hybridization
  • Microscopy, Confocal
  • Neurons/metabolism
  • Rhombencephalon/metabolism*
  • Spinal Cord/metabolism
  • Spinal Cord/pathology
  • Transcription, Genetic
  • Zebrafish
  • Zebrafish Proteins/metabolism*
PubMed
19536294 Full text @ PLoS One
Abstract
To better understand how individual genes and experience influence behavior, the role of a single homeotic unit, hoxb4a, was comprehensively analyzed in vivo by clonal and retrograde fluorescent labeling of caudal hindbrain neurons in a zebrafish enhancer-trap YFP line. A quantitative spatiotemporal neuronal atlas showed hoxb4a activity to be highly variable and mosaic in rhombomere 7-8 reticular, motoneuronal and precerebellar nuclei with expression decreasing differentially in all subgroups through juvenile stages. The extensive Hox mosaicism and widespread pleiotropism demonstrate that the same transcriptional protein plays a role in the development of circuits that drive behaviors from autonomic through motor function including cerebellar regulation. We propose that the continuous presence of hoxb4a positive neurons may provide a developmental plasticity for behavior-specific circuits to accommodate experience- and growth-related changes. Hence, the ubiquitous hoxb4a pleitropism and modularity likely offer an adaptable transcriptional element for circuit modification during both growth and evolution.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping