PUBLICATION

Defective Neuronal Positioning Correlates With Aberrant Motor Circuit Function in Zebrafish

Authors
Asante, E., Hummel, D., Gurung, S., Kassim, Y.M., Al-Shakarji, N., Palaniappan, K., Sittaramane, V., Chandrasekhar, A.
ID
ZDB-PUB-210714-4
Date
2021
Source
Frontiers in neural circuits   15: 690475 (Journal)
Registered Authors
Chandrasekhar, Anand
Keywords
axon guidance, behavior, facial branchiomotor neuron, food intake, jaw movement, neural circuits, neuronal migration, zebrafish
MeSH Terms
  • Zebrafish*
  • Neurogenesis
  • Axons
  • Cell Movement
  • Zebrafish Proteins/genetics
  • Motor Neurons*
  • Animals
(all 7)
PubMed
34248505 Full text @ Front. Neural Circuits
Abstract
Precise positioning of neurons resulting from cell division and migration during development is critical for normal brain function. Disruption of neuronal migration can cause a myriad of neurological disorders. To investigate the functional consequences of defective neuronal positioning on circuit function, we studied a zebrafish frizzled3a (fzd3a) loss-of-function mutant off-limits (olt) where the facial branchiomotor (FBM) neurons fail to migrate out of their birthplace. A jaw movement assay, which measures the opening of the zebrafish jaw (gape), showed that the frequency of gape events, but not their amplitude, was decreased in olt mutants. Consistent with this, a larval feeding assay revealed decreased food intake in olt mutants, indicating that the FBM circuit in mutants generates defective functional outputs. We tested various mechanisms that could generate defective functional outputs in mutants. While fzd3a is ubiquitously expressed in neural and non-neural tissues, jaw cartilage and muscle developed normally in olt mutants, and muscle function also appeared to be unaffected. Although FBM neurons were mispositioned in olt mutants, axon pathfinding to jaw muscles was unaffected. Moreover, neuromuscular junctions established by FBM neurons on jaw muscles were similar between wildtype siblings and olt mutants. Interestingly, motor axons innervating the interhyoideus jaw muscle were frequently defasciculated in olt mutants. Furthermore, GCaMP imaging revealed that mutant FBM neurons were less active than their wildtype counterparts. These data show that aberrant positioning of FBM neurons in olt mutants is correlated with subtle defects in fasciculation and neuronal activity, potentially generating defective functional outputs.
Genes / Markers
Figures
Figure Gallery (7 images)
Show all Figures
Expression
No data available
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
ch100TgTransgenic Insertion
    rw0TgTransgenic Insertion
      rw689
        		Point Mutation
        zf13TgTransgenic Insertion
          1 - 4 of 4
          Show
          Human Disease / Model
          No data available
          Sequence Targeting Reagents
          No data available
          Fish
          No data available
          Antibodies
          Orthology
          No data available
          Engineered Foreign Genes
          Marker Marker Type Name
          GFPEFGGFP
          mRFPEFGmRFP
          1 - 2 of 2
          Show
          Mapping
          No data available
          Your Input Welcome
          We welcome your input and comments. Please use this form to recommend updates to the information in ZFIN. We appreciate as much detail as possible and references as appropriate. We will review your comments promptly.
          Citation
          Asante, E., Hummel, D., Gurung, S., Kassim, Y.M., Al-Shakarji, N., Palaniappan, K., Sittaramane, V., Chandrasekhar, A. (2021) Defective Neuronal Positioning Correlates With Aberrant Motor Circuit Function in Zebrafish. Frontiers in neural circuits. 15:690475.