In the skin of zebrafish embryo, the vacuolar H+-ATPase (V-ATPase, H+ pump) distributed mainly in the apical membrane of H+-pump-rich cells, which pump internal acid out of the embryo and function similarly to acid-secreting intercalated cells in mammalian kidney. In addition to acid excretion, the electrogenic H+ efflux via the H +-ATPases in the gill apical membrane of freshwater fish was proposed to act as a driving force for Na+ entry through the apical Na + channels. However, convincing molecular physiological evidence in vivo for this model is still lacking. In this study, we used morpholino-modified antisense oligonucleotides to knockdown the gene product of H +-ATPase subunit A (atp6v1a) and examined the phenotype of the mutants. The H+-ATPase knockdown embryos revealed several abnormalities, including suppression of acid-secretion from skin, growth retardation, trunk deformation, and loss of internal Ca2+ and Na +. This finding reveals the critical role of H+-ATPase in embryonic acid-secretion and ion balance, as well.
|期刊||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|出版狀態||已發佈 - 五月 2007|
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