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Sterol-specific membrane interactions with the toxins from Karlodinium micrum (Dinophyceae) — a strategy for self-protection?
Abstract
The lipophilic toxins from Karlodinium micrum, KmTX, have negative effects on several co-occurring phytoplankton species, yet appear to have no effect on K. micrum itself. One of these compounds, KmTX2, has
differing toxicity towards eukaryotic membranes with differing sterol compositions (vertebrate > fungal > dinoflagellate). It is shown that KmTX2 causes lysis in a co-occurring potential grazer Oxyrrhis marina while
having no effect on K. micrum itself. K. micrum has a unique membrane sterol profile dominated by (24S)-4á- methyl-5á-ergosta-8(14),22-dien-3â-ol (gymnodinosterol), whereas O. marina was shown to possess 5,22- cholestadien-24â-methyl-3â-ol (brassicasterol) and 5- scholesten-3â-ol (cholesterol) as its major membrane sterols. In accord with toxicity data from whole cells containing these sterols, free sterols were found to inhibit haemolysis in the order cholesterol > ergosterol > gymnodinosterol. It appears that certain sterols can form stable complexes with the toxin molecule, thereby sequestering it away from erythrocyte membranes. It is concluded that K. micrum protects itself from the membrane-disrupting properties of its own toxins by possessing a membrane sterol that does not interact with these compounds.
differing toxicity towards eukaryotic membranes with differing sterol compositions (vertebrate > fungal > dinoflagellate). It is shown that KmTX2 causes lysis in a co-occurring potential grazer Oxyrrhis marina while
having no effect on K. micrum itself. K. micrum has a unique membrane sterol profile dominated by (24S)-4á- methyl-5á-ergosta-8(14),22-dien-3â-ol (gymnodinosterol), whereas O. marina was shown to possess 5,22- cholestadien-24â-methyl-3â-ol (brassicasterol) and 5- scholesten-3â-ol (cholesterol) as its major membrane sterols. In accord with toxicity data from whole cells containing these sterols, free sterols were found to inhibit haemolysis in the order cholesterol > ergosterol > gymnodinosterol. It appears that certain sterols can form stable complexes with the toxin molecule, thereby sequestering it away from erythrocyte membranes. It is concluded that K. micrum protects itself from the membrane-disrupting properties of its own toxins by possessing a membrane sterol that does not interact with these compounds.