Metamorphosis inHydractinia: Studies with activators and inhibitors aiming at protein kinase C and potassium channels.

Metamorphosis of planula larvae involves an activation of morphogenetically quiescent cells. The present work extends a previous study [Leitz T and Müller WA (1987) Dev Biol 121:82-89] on the participation of the phosphatidylinositol/diacylglycerol/protein kinase C system. Metamorphosis is stereospecifically induced by diacylglycerols, 1,2,-sn-dioctanoylglycerol (diC8) being by far the most effective substance. K-252a and sphingosine, inhibitors of mammalian protein kinases C, profoundly inhibited metamorphosis. Phorbolester-binding studies and the corresponding Scatchard plots revealed a specific and saturable binding of [3H]phorbol 12,13-dibutyrate to a single site of particulate fractions ofHydractinia with a specific binding affinityK d = 50 nM. K+ ionophores stimulated Cs+ - but inhibited diC8-induced metamorphoses, K+-channel blockers enhanced the inducing action of Cs+ or diC8. On the basis of these data and observations of others we propose that the activation ofHydractinia larvae takes place in some cells at the anterior end as a result of activation of a kinase-C-like enzyme, which directly or indirectly leads to the closure of K+ channels. Closure of these channels then causes depolarisation and, thus, release of an internal signal. This hypothesis unifies notions about the role of K+ channels and of the phosphatidylinositol system in initiation of metamorphosis inHydractinia.