Effects of dibutyryl cAMP and bacterial toxins on indoleamine-induced encystment of dinoflagellates.

Abstract

Dinoflagellates are the causative agents of red tides with worldwide occurrence and can be induced to encyst by in doleamines such as melatonin and 5-methoxytryptamine (5-MOT). This biological response may be mediated via indoleamine-binding proteins or receptors. Here we report the initial characterization of the signal transduction mechanisms by which indoleamines induce encystment of dinoflagellates. In particular, we explored the possible involvement of G proteins and cAMP in cyst formation. Both melatonin and 5-MOT promoted the encystment of Gonyaulax tamarensis and Crypthecodinium cohnii. Exposure of dinoflagellates to dibutyryl cAMP, which directly activates cAMP-dependent pathways, did not affect the ability of indoleamines to promote encystment. However, dibutyryl cAMP dose-dependently diminished the indoleamine-induced suppression of cell growth. Exposure of dinoflagellates to the bacterial toxins from Vibrio cholerae and Bordetella pertussis had no effect on the indoleamine-induced encystment response, indicating the lack of involvement of Gs or Gi-like proteins. Moreover, [32P]ADP ribosylation of dinoflagellate membranes by either toxin failed to identify substrate proteins. These results suggest that although the indoleamine-induced encystment of dinoflagellates may involve a G-protein-coupled signal transduction pathway, the identity of the G protein concerned may be distinct from those that regulate adenylyl cyclases in mammalian cells.