• Journal of Applied Biological Chemistry
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• v.59 no.3
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• pp.221-225
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• 2016

Tolaasin is a pore-forming peptide toxin produced by Pseudomonas tolaasii and causes a brown blotch disease by disrupting membrane structures of cultivated mushrooms. The mechanism and characteristics of tolaasin pore formation are not known in detail; however, tolaasin pores have been demonstrated in the artificial lipid bilayer. Since the tolaasin pore appeared less frequently and unstable in lipid bilayer, a mismatch between the length of tolaasin pore and the thickness of lipid membrane had been suggested. Therefore, tolaasin-induced hemolyses were measured by the additions of phospholipids composed of various fatty acids with different carbon numbers. When phosphatidylethanolamines made with two decanoic acids (C10:0, 1,2-didecanoyl-sn-glycero-3-phosphoethanolamine; DDPE), myristic acids (C14:0, 1,2-dimyristoyl-sn-glycero-3-phosphoethanolamine), and stearic acids (C18:0, 1,2-distearoyl-sn-glycero-3-phosphoethanolamine) were added to the buffer containing RBCs and tolaasin peptides, DDPE facilitated the tolaasin-induced hemolysis while the other two phospholipids showed no effects. At various concentrations of DDPE, the tolaasin-induced hemolysis was stimulated as a dose-dependent manner. The phospholipids composed of mediumchain fatty acids stabilize the tolaasin pore probably by binding between the pore structure and membrane phospholipids and making the membrane thickness thinner around the pore. These results showed that tolaasin molecules make more stable pores in the membrane made with phospholipids composed of medium length fatty acids, suggesting that the length of tolaasin pore is a little shorter than the thickness of RBC membrane.