ZFIN ID: ZDB-PUB-101004-1
Neuron-specific expression of atp6v0c2 in zebrafish CNS
Chung, A.Y., Kim, M.J., Kim, D., Bang, S., Hwang, S.W., Lim, C.S., Lee, S., Park, H.C., and Huh, T.L.
Date: 2010
Source: Developmental dynamics : an official publication of the American Association of Anatomists   239(9): 2501-2508 (Journal)
Registered Authors: Huh, Tae-Lin, Kim, Myoung-Jin, Park, Hae-Chul
Keywords: V-ATPase, neuron, Notch signaling, zebrafish
MeSH Terms:
  • Amino Acid Sequence
  • Animals
  • Central Nervous System/anatomy & histology
  • Central Nervous System/metabolism*
  • Humans
  • Molecular Sequence Data
  • Neurons/cytology
  • Neurons/metabolism*
  • Protein Isoforms/genetics
  • Protein Isoforms/metabolism*
  • Protein Subunits/genetics
  • Protein Subunits/metabolism*
  • Receptors, Notch/genetics
  • Receptors, Notch/metabolism
  • Sequence Alignment
  • Signal Transduction/physiology
  • Vacuolar Proton-Translocating ATPases/genetics
  • Vacuolar Proton-Translocating ATPases/metabolism*
  • Zebrafish*/anatomy & histology
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 20839327 Full text @ Dev. Dyn.
Vacuolar ATPase (V-ATPase) is a multi-subunit enzyme that plays an important role in the acidification of a variety of intracellular compartments. ATP6V0C is subunit c of the V(0) domain that forms the proteolipid pore of the enzyme. In the present study, we investigated the neuron-specific expression of atp6v0c2, a novel isoform of the V-ATPase c-subunit, during the development of the zebrafish CNS. Zebrafish atp6v0c2 was isolated from a genome-wide analysis of the zebrafish mib(ta52b) mutant designed to identify genes differentially regulated by Notch signaling. Whole-mount in situ hybridization revealed that atp6v0c2 is expressed in a subset of CNS neurons beginning several hours after the emergence of post-mitotic neurons. The ATP6V0C2 protein is co-localized with the presynaptic vesicle marker, SV2, suggesting that it is involved in neurotransmitter storage and/or secretion in neurons. In addition, the loss-of-function experiment suggests that ATP6V0C2 is involved in the control of neuronal excitability.