Ammonia, tetraethylammonium, barium and amiloride induce metamorphosis in the marine hydroid Hydractinia.

In Hydractinia metamorphosis from the swimming larval stage to the sessile polyp stage has been found to be inducible by several agents, including Li+, K+, Cs+, Rb+, diacylglycerol (DG), tetradecanoyl-phorbol-acetate (TPA) and some other tumour-promoting phorbol esters. Induction is antagonized by ouabain and compounds which are able to increase the internal level of S-adenosylmethionine (SAM). Based on the finding that Hydractinia larvae contain such compounds in a stored form, including N-methylpicolinic acid, N-methylnicotinic acid and N-trimethylglycine, as well as on the results of experiments with antagonists of SAM production and transmethylation, it has been argued that regulation of the internal SAM level plays a key role in the control of metamorphosis. However, it remains to be clarified whether the inducing agents act by decreasing the SAM level or by via different pathways. In the present study, substances chemically related to the substances known to induce or inhibit metamorphosis were tested for their metamorphosis-inducing abilities. Some were found to be effective, including NH4+, methylamine, tetraethylammonium ions (TEA+), ethanolamine, Ba2+, Sr2+ and the diuretic, amiloride. It is of particular interest that in many organisms TPA and DG increase cytoplasmic pH while amiloride prevents a rise in pHi. Several of the substances known to trigger metamorphosis may increase the internal NH4+ concentration by hindering the export of the constantly produced NH4+ through K+ channels or through the Na+-H+ antiport. Treatment with Cs+ for 1 h increases the internal level of NH4+. Produced and applied ammonia, as well as applied methylamine and ethanolamine, may act by accepting methyl groups, thus reducing the SAM level.