ZFIN ID: ZDB-PUB-080801-5
Zebrafish orthologue of mental retardation protein IL1RAPL1 regulates presynaptic differentiation
Yoshida, T., and Mishina, M.
Date: 2008
Source: Molecular and cellular neurosciences   39(2): 218-228 (Journal)
Registered Authors: Mishina, Masayoshi, Yoshida, Tomoyuki
Keywords: none
MeSH Terms:
  • Animals
  • Cell Differentiation/drug effects
  • Cell Differentiation/physiology*
  • Cloning, Molecular/methods
  • Embryo, Nonmammalian
  • GAP-43 Protein/genetics
  • GAP-43 Protein/metabolism
  • Gene Expression Profiling/methods
  • Green Fluorescent Proteins/genetics
  • Interleukin-1 Receptor Accessory Protein/genetics
  • Interleukin-1 Receptor Accessory Protein/physiology*
  • Microinjections/methods
  • Molecular Chaperones/genetics
  • Molecular Chaperones/metabolism
  • Olfactory Receptor Neurons/cytology*
  • Olfactory Receptor Neurons/physiology
  • Oligodeoxyribonucleotides, Antisense/pharmacology
  • Presynaptic Terminals/drug effects
  • Presynaptic Terminals/metabolism*
  • Synaptic Vesicles/drug effects
  • Synaptic Vesicles/physiology
  • Transcription, Genetic/physiology
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed: 18657618 Full text @ Mol. Cell Neurosci.
IL1-receptor accessory protein-like 1 (IL1RAPL1), a member of interleukine-1/toll receptor (TIR) family, is responsible for a nonsyndromic form of mental retardation (MR). The zebrafish orthologue of mammalian IL1RAPL1, designated as IL1RAPL 1B, was expressed widely in the brain and in the olfactory placode. We employed an olfactory sensory neuron-specific gene manipulation system in combination with in vivo imaging of transparent zebrafish embryos to examine the functional role of IL1RAPL 1B in synaptic vesicle accumulation and subsequent morphological remodeling of axon terminals, the characteristic features of presynaptic differentiation of zebrafish olfactory sensory neurons during synapse formation. Antisense morpholino oligonucleotide against IL1RAPL 1B suppressed both the synaptic vesicle accumulation and axon terminal remodeling. Consistently, the overexpression of IL1RAPL 1B stimulated synaptic vesicle accumulation. Swapping the carboxyl-terminal domain of IL1RAPL 1B with that of mouse IL-1 receptor accessory protein abolished the stimulatory effect. On the other hand, a substitution mutation in the TIR domain suppressed the morphological remodeling of axon terminals. Thus, the regulation of synaptic vesicle accumulation and subsequent morphological remodeling by IL1RAPL 1B appeared to be mediated by distinct domains. These results suggest that IL1RAPL 1B plays an important role in presynaptic differentiation during synapse formation.