Vanadate, known to interfere with signal transduction, induces metamorphosis in Hydractinia (Coelenterata; Hydrozoa) and causes profound alterations of the larval and postmetamorphic body pattern

Abstract. 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 immuno-histochemistry 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 m M ort-hovanadate and 25–250 m M 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.