Biogenesis of GPI-anchored proteins is essential for surface expression of sodium channels in zebrafish Rohon-Beard neurons to respond to mechanosensory stimulation

  • Yuri Nakano
    Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
  • Morihisa Fujita
    Department of Immunoregulation, Research Institute for Microbial Disease, Osaka University, Suita 565-0871, Japan
  • Kazutoyo Ogino
    Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
  • Louis Saint-Amant
    Départment de Pathologie et Biologie Cellulaire, Université de Montréal, Montréal, QC H3T 1J4, Canada
  • Taroh Kinoshita
    Department of Immunoregulation, Research Institute for Microbial Disease, Osaka University, Suita 565-0871, Japan
  • Yoichi Oda
    Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan
  • Hiromi Hirata
    Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan

書誌事項

公開日
2010-05-15
資源種別
journal article
DOI
  • 10.1242/dev.047464
  • 10.1016/j.neures.2010.07.096
公開者
The Company of Biologists

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説明

<jats:p>In zebrafish, Rohon-Beard (RB) neurons are primary sensory neurons present during the embryonic and early larval stages. At 2 days post-fertilization (dpf), wild-type zebrafish embryos respond to mechanosensory stimulation and swim away from the stimuli, whereas mi310 mutants are insensitive to touch. During ~2-4 dpf, wild-type RB neurons undergo programmed cell death, which is caused by sodium current-mediated electrical activity, whereas mutant RB cells survive past 4 dpf, suggesting a defect of sodium currents in the mutants. Indeed, electrophysiological recordings demonstrated the generation of action potentials in wild-type RB neurons, whereas mutant RB cells failed to fire owing to the reduction of voltage-gated sodium currents. Labeling of dissociated RB neurons with an antibody against voltage-gated sodium channels revealed that sodium channels are expressed at the cell surface in wild-type, but not mutant, RB neurons. Finally, in mi310 mutants, we identified a mis-sense mutation in pigu, a subunit of GPI (glycosylphosphatidylinositol) transamidase, which is essential for membrane anchoring of GPI-anchored proteins. Taken together, biogenesis of GPI-anchored proteins is necessary for cell surface expression of sodium channels and thus for firings of RB neurons, which enable zebrafish embryos to respond to mechanosensory stimulation.</jats:p>

収録刊行物

  • Development

    Development 137 (10), 1689-1698, 2010-05-15

    The Company of Biologists

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