Fig. 6

Fig. 6

Hypotheses for Gv signalling pathways in three developmental stages. Arrows may represent several molecular steps. Red color indicates block (red crosses) or decrease in the mutant, blue depicts an increase, green represents wildtype levels, magenta shows hypothetical effect. (a) In the mutant embryo decreased levels of NKA.5 (Na⁺/K⁺ ATPase) and NCX (NCX1b) might secondarily influence Zn²⁺ levels in the hatching gland, possibly via two zinc transporters present in hatching gland cells [39], which would influence hatching enzyme activity, leading to premature hatching. (b) Top row shows wildtype situation: Gv is activated by so far unknown ligand/receptor pairs and eventually regulates NKA.5 and NCX expression, which is required for proper cartilage formation (upper zebrafish larva). Pm, plasma membrane; ec, extracellular; ic, intracellular; numbers refer to temporal order. Bottom row shows mutant situation, red crosses depict losses of the respective elements; red arrow, downregulation of expression of Na⁺/K⁺ ATPase and NCX may lead to reduced and distorted cartilage formation (lower zebrafish larva). Note that reduced calcium extrusion means less calcium getting inside the animal via the basal surface of ionocytes. For details of larval micrographs see Fig. 4b legend. (c) In the mutant adult kidney four ion transporters act to some extent compensatory: A decrease in SLC26 may be balanced by an increase in NCC for the chloride level, and sodium levels are reduced by increased NKA.5, but augmented by increased NCC and NCX. Such compensatory effects may explain the absence of outwardly visible phenotype in adult mutant zebrafish (framed inset)