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Updated: Mar 23, 2026

Deciphering the Molecular Mechanism and Function of Pore-Forming Toxins Using Leishmania major
Published on: October 28, 2022
DINOFLAGELLATE HOST-PARASITE STEROL PROFILES DICTATE KARLOTOXIN SENSITIVITY(1)
Allen R Place1, Xuemei Bai1, Sunju Kim1
1Center of Marine Biotechnology, University of Maryland Biotechnology Institute, 701 E. Pratt Street, Baltimore, Maryland 21202, USAThe Smithsonian Environmental Research Center, PO Box 28, 647 Contees Wharf Rd. Edgewater, Maryland 21037, USA.
Abstract:
We examined the sterol profile of Karlodinium veneficum (D. Ballant.) J. Larsen, Akashiwo sanguinea (Hiraska) Ge. Hansen et Moestrup, Alexandrium tamarense (M. Lebour) Balech, Alexandrium affine (H. Inoue et Fukuyo) Balech, Gonyaulax polygramma F. Stein, and Gymnodinium instriatum (Freud. et J. J. Lee) Coats, along with their Amoebophyra parasites. There were no consistent sterol profiles that characterized the genus Amoebophyra. Instead, in five out of six comparisons, the host and parasite sterol profiles where highly correlated. The one exception, Amoebophyra sp. ex Alex. tamarense, was least like its host in sterol profile and also possessed the widest host range for infection. There was little correlation between host and parasite in fatty acid profiles, with the parasite being deficient in fatty acids characteristic of the plastid [e.g., 18:5(n-3) associated with galactolipids of the thylakoids, as previously published by Adolf et al. (2007)]. Those hosts and parasites with sterol profiles dominated by desmethyl sterols were most sensitive to karlotoxin toxicity. In the host-parasite pairs most sensitive to karlotoxin addition, recovery of the intact karlotoxin molecule was poorest. Given the sensitivity to karlotoxin, some species of Amoebophyra may avoid infection of K. veneficum.

