PUBLICATION

Overexpression of Wld(s) or Nmnat2 in mauthner cells by single-cell electroporation delays axon degeneration in live zebrafish

Authors
Feng, Y., Yan, T., Zheng, J., Ge, X., Mu, Y., Zhang, Y., Wu, D., Du, J.L., and Zhai, Q.
ID
ZDB-PUB-101004-29
Date
2010
Source
Journal of neuroscience research   88(15): 3319-3327 (Journal)
Registered Authors
Du, Jiu Lin
Keywords
Nmnat2, Wallerian degeneration, axon degeneration, neurodegeneration
MeSH Terms
  • Animals
  • Axons/metabolism*
  • Axons/pathology
  • Electroporation
  • HEK293 Cells
  • Humans
  • Immunoprecipitation
  • Microscopy, Confocal
  • Nerve Degeneration/genetics
  • Nerve Degeneration/metabolism*
  • Nerve Degeneration/pathology
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism*
  • Nicotinamide-Nucleotide Adenylyltransferase/genetics
  • Nicotinamide-Nucleotide Adenylyltransferase/metabolism*
  • Zebrafish
PubMed
20857515 Full text @ J. Neurosci. Res.
Abstract
Axon degeneration is supposed to be a therapeutic target for treating neurodegenerative diseases. Mauthner cells (M-cells) are ideal for studying axons in vivo because of their limited numbers, large size, and long axons. In this study, we labeled M-cells by single-cell electroporation with plasmids expressing DsRed2 or EGFP. Injury-induced axon degeneration in labeled M-cell was imaged under a confocal microscope, and we found that the Mauthner axons started to degenerate about 24 hr after lesion. The Wld(S) protein containing full-length Nmnat1 is well-known for its axon-protective function in many systems. Overexpression of Wld(S) in M-cells also greatly delayed axon degeneration in live zebrafish. Nmnat2 is the only Nmnat highly expressed in brain. Here we demonstrated that overexpression of Nmnat2 in M-cells significantly delayed axon degeneration in vivo, and disruption of the NAD synthesis activity of Nmnat2 markedly attenuated its axon-protective function. All these data show that injury-induced axon degeneration of M-cell has a mechanism similar to that in mammalians and would be a valuable model for studying axon degeneration in vivo.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping