VANADATE, KNOWN TO INTERFERE WITH SIGNAL TRANSDUCTION, INDUCES METAMORPHOSIS IN HYDRACTINIA (COELENTERATA, HYDROZOA) AND CAUSES PROFOUND ALTERATIONS OF THE LARVAL AND POSTMETAMORPHIC BODY PATTERN

Vanadate interferes with the development of planula larvae of the marine hydrozoon Hydractinia echinata. Exposure of embryos (morulae) to vanadate leads to teratomalike and heavily malformed larvae. Thirty h old embryos treated for 18 h develop into larvae signficiantly longer than control larvae. In control larvae cell proliferation detected by BrdU-antiBrdU immunohistochemistry ceases at the posterior and anterior pole at an age of 72 h but is maintained at a high level in treated larvae. Even in teratomas cell proliferation is at a higher level than in proliferation zones of control animals indicating a deregulation of proliferation in the treated larvae just as in mammalian teratomas. Arginine-phenylalanine-amide (RF-amide) immunopositive nerve cells and fibres are found in 5 day old teratomas. RF-amide immunopositive cells are concentrated in globular structures. The animals overcome the deregulation by extruding these structures. In intact larvae 2-4 mM orthovanadate and 25-250 mM metavanadate induced metamorphosis. A majority of the developing polyps displayed an abnormal body pattern often having an elongated hypostome and instead of one whorl, had several tentacle whorls, one upon another. Incomplete polyps with a larval anterior part instead of a basal plate are also observed. Metamorphosis induced by vanadate is promoted by amiloride and inhibited by ouabain. Vanadate also disturbs pattern control in regeneration. Up to 50% of isolated larval tails either regenerate a second mirror-image tail instead of an anterior one or develop tentacles at their anterior part (up to 20%), i.e., exhibited a reversed polarity. Vanadate is assumed to act by influencing signal transducing pathways like the phosphoinositide cycle or tyrosine phosphorylation.