PUBLICATION

Expression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafish

Authors
Schweitzer, J., Becker, T., Becker, C.G., and Schachner, M.
ID
ZDB-PUB-030116-4
Date
2003
Source
Glia   41(3): 301-317 (Journal)
Registered Authors
Becker, Catherina G., Becker, Thomas, Schachner, Melitta, Schweitzer, Jörn
Keywords
none
MeSH Terms
  • Age Factors
  • Animals
  • Cloning, Molecular
  • Gene Expression Regulation, Developmental
  • Molecular Sequence Data
  • Myelin P0 Protein/genetics*
  • Myelin P0 Protein/metabolism
  • Myelin Sheath/physiology
  • Nerve Crush
  • Nerve Fibers, Myelinated/physiology
  • Nerve Regeneration/physiology*
  • Oligodendroglia/physiology*
  • Optic Nerve/cytology
  • Optic Nerve/physiology*
  • RNA, Messenger/analysis
  • Rhombencephalon/cytology
  • Rhombencephalon/physiology
  • Sequence Homology, Amino Acid
  • Spinal Cord/cytology
  • Spinal Cord/physiology*
  • Zebrafish
PubMed
12528184 Full text @ Glia
Abstract
The immunoglobulin superfamily molecule protein zero (P0) is important for myelin formation and may also play a role in adult axon regeneration, since it promotes neurite outgrowth in vitro. Moreover, it is expressed in the regenerating central nervous system (CNS) of fish, but not in the nonregenerating CNS of mammals. We identified a P0 homolog in zebrafish. Cell type-specific expression of P0 begins in the ventromedial hindbrain and the optic chiasm at 3-5 days of development. Later (at 4 weeks) expression has spread throughout the optic system and spinal cord. This is consistent with a role for P0 in CNS myelination during development. In the adult CNS, glial cells constitutively express P0 mRNA. After an optic nerve crush, expression is increased within 2 days in the entire optic pathway. Expression peaks at 1 to 2 months and remains elevated for at least 6 months postlesion. After enucleation, P0 mRNA expression is also upregulated but fails to reach the high levels observed in crush-lesioned animals at 4 weeks postlesion. Spinal cord transection leads to increased expression of P0 mRNA in the spinal cord caudal to the lesion site. The glial upregulation of P0 mRNA expression after a lesion of the adult zebrafish CNS suggests roles for P0 in promoting axon regeneration and remyelination after injury.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping