SMT - Studying Interaction of Cyclopeptyde Toxins with Lipid Bilayer


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PHILIP A. GURNEV

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Studying Interaction of Cyclopeptyde Toxins with Lipid Bilayer

Amphyphilic toxins from Pseudomonas syringae are known to form well-defined channels in planar lipid bilayers. To form a channel, toxin recruits lipid molecules from the host bilayer. Focusing on conductance and gating properties of these channels, we learn about physical properties of lipid bilayer, e.g. surface charge, elastic stress, etc. [PDF], [PDF]

Molecular structure of syringomycin E (SRE), the major component of Pseudomonas syringae pv. syringae toxin. Nine amino acid residues (mostly polar) are enclosed into the lactone ring with the attached hydrocarbon chain. Image courtesy of O. S. Ostroumova.

Voltage gating of SRE-induced ion channels is regulated by the surface charge of a lipid bilayer. In a negatively charged bilayer, channel opening (current increase) is favored by positive transmembrane voltage, while negative voltage stimulates channel closure (A). The dependence of channel gating on voltage is clearly opposite when surface charge is reduced either by protonation (B), screening by high salt concentration (C), or substitution of charged lipid with uncharged one (D).

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Collaborators:

	Ludmila V. Schagina
	Valery V. Malev
	Jon Y. Takemoto

Voltage gating of SRE-induced ion channels is regulated by the surface charge of a lipid bilayer. In a negatively charged bilayer, channel opening (current increase) is favored by positive transmembrane voltage, while negative voltage stimulates channel closure (A). The dependence of channel gating on voltage is clearly opposite when surface charge is reduced either by protonation (B), screening by high salt concentration (C), or substitution of charged lipid with uncharged one (D). From [PDF]

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