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THE ROLE OF CALCIUM IN FLOW‐STIMULATED BIOLUMINESCENCE OF THE RED TIDE DINOFLAGELLATE LINGULODINIUM POLYEDRUM
Author(s) -
Von Dassow P.,
Latz M.I.
Publication year - 2000
Publication title -
journal of phycology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.85
H-Index - 127
eISSN - 1529-8817
pISSN - 0022-3646
DOI - 10.1046/j.1529-8817.1999.00001-204.x
Subject(s) - biology , mechanotransduction , aequorin , bioluminescence , calcium , biophysics , calcium channel , microbiology and biotechnology , biochemistry , chemistry , intracellular , organic chemistry
Many marine planktonic dinoflagellates emit flashes of light in response to either laminar or turbulent flows as well as direct mechanical stimulation. The production of a flash of light is known to be mediated by a proton‐mediated action potential across the vacuolar membrane; the mechanotransduction process initiating this action potential is unknown. Here we report on an investigation into the role of Ca +2 in the mechanotransduction process regulating bioluminescence in the red tide dinoflagellate Lingulodinium polyedrum. Calcium ionophores and low concentrations of the membrane‐disrupting agent digitonin stimulated bioluminescence only when calcium was present in the media or added with the agent, indicating that the flash‐triggering vacuolar action potential is specifically stimulated by a calcium influx. A variety of known calcium channel blockers or antagonists inhibited mechanically stimulated bioluminescence but did not affect cellular bioluminescent capacity. In many cases the inhibitory affect occurred after only a brief exposure. In addition, gadolinium (Gd +3 ), a blocker of many stretch‐activated ion channels, caused potent inhibition of mechanically stimulated bioluminescence. The order of potency of the transition metals tested was La +3 > Gd +3 > Co +2 > Mn +2 > Ni +2 , similar to their potency as blockers of known calcium channels. Experiments with a quantified shear flow demonstrated that flow‐stimulated bioluminescence depended on the level of extracellular calcium. Future work will elucidate the signaling pathway involving calcium‐mediated flow‐stimulated mechanotransduction. Our goal is to use bioluminescence as a proxy for the initial cellular mechanotransduction events triggered by fluid flow.