PUBLICATION

Mechanism of development of ionocytes rich in vacuolar-type H(+)-ATPase in the skin of zebrafish larvae

Authors
Esaki, M., Hoshijima, K., Nakamura, N., Munakata, K., Tanaka, M., Ookata, K., Asakawa, K., Kawakami, K., Wang, W., Weinberg, E.S., and Hirose, S.
ID
ZDB-PUB-090310-19
Date
2009
Source
Developmental Biology   329(1): 116-129 (Journal)
Registered Authors
Hoshijima, Kazuyuki, Kawakami, Koichi, Tanaka, Mikiko, Weinberg, Eric
Keywords
Mitochondria-rich cell, Foxi1, Foxi3a, Gcm2, Positive feedback loop, Zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Fluorescent Antibody Technique, Indirect
  • Immunohistochemistry
  • In Situ Hybridization
  • Keratinocytes/cytology
  • Keratinocytes/metabolism*
  • Larva/metabolism*
  • Microinjections
  • Mitochondria/metabolism*
  • Models, Biological
  • Oligonucleotides, Antisense/pharmacology
  • Proton-Translocating ATPases/metabolism*
  • Skin/cytology
  • Skin/metabolism*
  • Vacuoles/genetics
  • Vacuoles/metabolism*
  • Zebrafish/genetics
  • Zebrafish/metabolism
PubMed
19268451 Full text @ Dev. Biol.
Abstract
Mitochondrion-rich cells (MRCs), or ionocytes, play a central role in aquatic species, maintaining body fluid ionic homeostasis by actively taking up or excreting ions. Since their first description in 1932 in eel gills, extensive morphological and physiological analyses have yielded important insights into ionocyte structure and function, but understanding the developmental pathway specifying these cells remains an ongoing challenge. We previously succeeded in identifying a key transcription factor, Foxi3a, in zebrafish larvae by database mining. In the present study, we analyzed a zebrafish mutant, quadro (quo), deficient in foxi1 gene expression and found that foxi1 is essential for development of an MRC subpopulation rich in vacuolar-type H(+)-ATPase (vH-MRC). foxi1 acts upstream of Delta-Notch signaling that determines sporadic distribution of vH-MRC and regulates foxi3a expression. Through gain-and loss-of-function assays and cell transplantation experiments, we further clarified that (1) the expression level of foxi3a is maintained by a positive feedback loop between foxi3a and its downstream gene gcm2 and (2) Foxi3a functions cell-autonomously in the specification of vH-MRC. These observations provide a better understanding of the differentiation and distribution of the vH-MRC subtype.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes