FGF-activated calcium channels control neural gene expression in Xenopus

In vertebrates, the formation of the nervous system starts at gastrulation with a process called neural induction. This process requires, at least in part, the inhibition of BMP signalling in the ectoderm by noggin, as well as FGF receptor activation and Ca2+ signalling. Our studies with Xenopus embryos suggest that an increase in intracellular Ca2+ concentration ([Ca2+]i), via dihydropyridine-sensitive Ca2+ channels (DHP-sensitive Ca2+ channels) is necessary and sufficient to direct the ectodermal cells toward a neural fate, and that Ca2+ directly controls the expression of neural genes. The mechanism by which the DHP-sensitive Ca2+ channels are activated during neural induction remains unknown. One possible mechanism is via the activation of FGF signalling. Using isolated ectoderm tissue, here we demonstrated that FGF-4 depolarises the membrane of ectodermal cells and induces an increase in [Ca2+]i. This Ca2+ increase can be blocked by SU5402, an FGF receptor inhibitor, and by DHP-sensitive Ca2+ channel antagonists. These inhibitors also block the induction of neural genes. We discuss a possible gating mechanism for the activation of DHP-sensitive Ca2+ channels via the FGF signalling pathway, which involves arachidonic acid and TRPC1 channel activation.