PHYTOTOXICITY OF FUMONISINS AND RELATED-COMPOUNDS

The fumonisins and AAL-toxin are related long-chain alkylamines with propane carboxylic acid moieties. The fumonisins, especially fumonisin B1 (FB1), were initially described as mammalian toxins; however, they are also potent phytotoxins. The fumonisins have a spectrum of susceptible plant species similar to that of AAL-toxin. The aminopentol derivatives of the B fumonisins are generally less toxic than the parent compounds, while the A series of fumonisins (acetylated forms) are essentially inactive. AAL-toxin was first thought to be host-specific for certain tomato cultivars, but now is known to affect many weed and crops species. Monocotyledonous species are less affected than dicotyledonous species. Tomatoes with the asc/asc genotype, jimsonweed, black nightshade, and duckweeds are the most susceptible species tested thus far. FB1 causes toxicity on contact with plant tissue and at sites distal from wounds, demonstrating xylem mobility. AAL-toxin is an important virulence factor for infection of certain susceptible tomato cultivars by Alternaria alternata f. sp. lycopersici. Ultrastructural studies show that FB1 and AAL-toxin both cause rapid plasma membrane disruption. Both FB1 and AAL-toxin are thought to interfere with plasma membrane function through disruption of sphingolipid metabolism by inhibition of sphinganine (sphingosine) N-acyltransferase (ceramide synthase), the same mechanism of toxicity as in animals. As in animals, high levels of ceramide synthase precursors accumulate in fumonisin- and AAL-toxin-treated plants. In addition, high concentrations of long chain sphingoid bases applied to plants cause phytotoxicity symptoms similar to those of fumonisins and AAL-toxin. Thus, the phytotoxicity of fumonisins and AAL-toxin are likely to be due to the accumulation of phytotoxic sphingolipid intermediates.