CELLULAR AND INTRACELLULAR PATHWAYS MEDIATING THE METAMORPHIC STIMULUS IN HYDROZOAN PLANULAE

Both the natural metamorphic stimulus (an unidentified bacterial product) and an artificial trigger of metamorphosis (Cs+) cause large calcium transients in planula cells of the hydrozoan Mitrocomella polydiademata. When these transients are inhibited with calcium channel blockers, metamorphosis is also inhibited. All cells of the Mitrocomella planula contain a calcium-specific photoprotein. The cells where the calcium transients occur during natural- and Cs+-induced metamorphosis have been visualized in normal and entoderm free planulae that lack ganglion cells, using a compound microscope coupled to an image intensifier and video camera. During bacteria- and Cs+-induced metamorphosis, groups of contiguous cells, occupying from about 10% to the entire visible surface of the planula, simultaneously exhibit calcium transients. When the cells that initiate a transient comprise only part of the planula surface, the calcium transient frequently propagates and can eventually involve every cell on the visible planula surface. There is no special site on the planula surface where calcium transients are more apt to be initiated. There is no indication that propagation of a flash in one direction is more likely than in another. The velocity of propagation is virtually the same in all directions. The only feature of the spatial distribution of bacteria- and Cs+-induced calcium transients that appears to be necessary for the induction of metamorphosis is that at least one transient must involve all of the surface cells of the planula. The spatial behavior of calcium transients is the same in entoderm free planulae (lacking ganglion cells) as in normal planulae. The propagation of these calcium transients most probably occurs via epithelial conduction. This metamorphic step involving calcium transients is probably the intercellular communication system that informs the cells of the planula that metamorphosis will commence. Metamorphosis in Mitrocomella planulae can also be induced with phorbol esters. Calcium transients do not occur during phorbol ester-induced metamorphosis, indicating that they act at a different point in the metamorphic pathway. Calcium channel blockers do not inhibit phorbol ester-induced metamorphosis. Inhibitors of protein kinase-C, inhibit both phorbol ester-induced metamorphosis and Cs+- and bacteria-induced metamorphosis, but have no effect on the calcium transients induced by Cs+. This indicates that the calcium transient mediated step in the metamorphic pathway occurs prior to protein kinase-C activation. Calcium transients probably play a major role in activating protein kinase-C. © 1990 Springer-Verlag.