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STIMULATION OF BIOLUMINESCENCE IN DINOFLAGELLATES BY RED LIGHT *
Author(s) -
Sweeney Beatrice M.,
Fork David C.,
Satoh Kazuhiko
Publication year - 1983
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1983.tb04499.x
Subject(s) - dcmu , bioluminescence , action spectrum , light emission , biophysics , photosynthesis , photosystem ii , dinoflagellate , light intensity , chemistry , photochemistry , biology , biochemistry , botany , physics , optoelectronics , optics
In three species of dinoflagellate, Gonyaulax polyedra, Pyrocyslis fusiformis and Pyrocvstis lunula , bioluminescence can be stimulated by light. This phenomenon is observed if the cell suspension is rendered anaerobic by any of the following treatments: N 2 gas. metabolically active yeast. glucose plus glucose oxidase, dithionite or allowing a concentrated cell suspension to stand for several hours in darkness, conditions which remove oxygen from the cell suspension. An alternate pretreatment is inclusion of carbonylcyanide‐m‐chlorophenyl hydrazone or hydroxylamine in the cell suspension. The emission spectrum with a maximum at 478 nm identifies dinoflagellate luciferin as the emitter. The action spectrum (maximum at 675 nm in the red region of the spectrum) points to chlorophyll as the photoreceptor. Evidence for the participation of PS II of photosynthesis in the light‐stimulation of bioluminescence is the strong inhibition of light emission by 3‐(3.4‐dichlorophenyl)‐l.l‐dimethylurca (DCMU) and 2,5‐dibromo‐3‐isopropyl‐p‐benzoquinone and the failure of diaminodurol + ascorbate to reverse the inhibition by DCMU. The observation that, with short irradiations (5 μ.s). no bioluminescence is emitted until the third flash also suggests photosystem II (PS II) as the site of stimulation. The evolution of oxygen is not involved in the light‐stimulation of bioluminescence. since oxygen evolution is completely inhibited by NH 2 OH, while light emission is potentiated by the presence of NH 2 OH. A consideration of the action of inhibitors suggests that the stimulation of light emission is the result of a change in membrane potential produced upon irradiation of PS II. This membrane potential is not caused by the movement of protons.