Channel formation in phospholipid bilayer membranes by the toxin ofHeminthosporium maydis, race T

Abstract

Southern Corn Leaf Blight is caused by a toxin produced by a virulent form ofHelminthosporium maydis (Race T). The toxin has been shown to uncouple oxidative phosphorylation and dissipate Ca2+ gradients in mitochondria isolated from susceptible, but not resistant, corn. The possibility that the toxin acted by increasing the permeability of membranes to ions was tested using a planar bilayer membrane system. Addition of the toxin to the bilayer system, under voltage-clamp conditions, resulted in stepwise increases in current across the phospholipid bilayer, a response characteristic for channel formers. Single-channel conductance in 1m KCl is 27 pS which corresponds to 1.7×107 ions sec−1 channel−1 at 100 mV applied potential. The toxin channels are: (i) fairly uniform in conductance, (ii) ideally selective for K+ over Cl−, and (iii) most conductive to H+. The channel showed the following selectivity for alkali metal cations: Rb+>K+>Cs+>Na+>Li+ (16∶9∶7∶3∶1) based on the most frequently observed conductance in 1m chloride salts. The toxin showed no voltage dependence over the range of −100 to +100 mV. Channel formation was also a property of a synthetic analog (Cmpd IV) of the toxin. The ability of the native toxin to form channels may be a mode of toxin action on mitochondrial membranes from susceptible corn.