Kwong, R.W., Kumai, Y., and Perry, S.F. (2013) Evidence for a role of tight junctions in regulating sodium permeability in zebrafish (Danio rerio) acclimated to ion-poor water. Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology. 183(2):203-213.
Freshwater teleosts are challenged by diffusive ion loss across permeable epithelia including gills and skin. Although the
mechanisms regulating ion loss are poorly understood, a significant component is thought to involve paracellular efflux through
pathways formed via tight junction proteins. The mammalian orthologue (claudin-4) of zebrafish (Danio rerio) tight junction protein, claudin-b, has been proposed to form a cation-selective barrier regulating the paracellular loss
of Na+. The present study investigated the cellular localization and regulation of claudin-b, as well as its potential contribution
to Na+ homeostasis in adult zebrafish acclimated to ion-poor water. Using a green fluorescent protein-expressing line of transgenic
zebrafish, we found that claudin-b was expressed along the lamellar epithelium as well as on the filament in the inter-lamellar
regions. Co-localization of claudin-b and Na+/K+-ATPase was observed, suggesting its interaction with mitochondrion-rich cells. Claudin-b also appeared to be associated with
other cell types, including the pavement cells. In the kidney, claudin-b was expressed predominantly in the collecting tubules.
In addition, exposure to ion-poor water caused a significant increase in claudin-b abundance as well as a decrease in Na+ efflux, suggesting a possible role for claudin-b in regulating paracellular Na+ loss. Interestingly, the whole-body uptake of a paracellular permeability marker, polyethylene glycol-400, increased significantly
after prolonged exposure to ion-poor water, indicating that an increase in epithelial permeability is not necessarily coupled
with an increase in passive Na+ loss. Overall, our study suggests that in ion-poor conditions, claudin-b may contribute to a selective reduction in passive
Na+ loss in zebrafish.