Gutiérrez-Nájera Nora A, Saucedo-García Mariana, Noyola-Martínez Liliana, Vázquez-Vázquez Christian, Palacios-Bahena Silvia, Carmona-Salazar Laura, Plasencia Javier, El-Hafidi Mohammed, Gavilanes-Ruiz Marina
Instituto Nacional de Medicina Genómica. Periférico Sur 4124, Torre 2, 5° piso. Álvaro Obregón 01900, Cd. de México, Mexico.
Instituto de Ciencias Agropecuarias, Universidad Autónoma del Estado de Hidalgo, Avenida Universidad Km. 1, Rancho Universitario, Tulancingo-Santiago, Tulantepec, Tulancingo 43600, Hidalgo, Mexico.
Plants (Basel). 2020 Jan 23;9(2):150. doi: 10.3390/plants9020150.
Fumonisin B1 is a mycotoxin produced by that modifies the membrane properties from animal cells and inhibits complex sphingolipids synthesis through the inhibition of ceramide synthase. The aim of this work was to determine the effect of Fumonisin B1 on the plant plasma membrane when the mycotoxin was added to germinating maize embryos. Fumonisin B1 addition to the embryos diminished plasma membrane fluidity, increased electrolyte leakage, caused a 7-fold increase of sphinganine and a small decrease in glucosylceramide in the plasma membrane, without affecting phytosphingosine levels or fatty acid composition. A 20%-30% inhibition of the plasma membrane H-ATPase activity was observed when embryos were germinated in the presence of the mycotoxin. Such inhibition was only associated to the decrease in glucosylceramide and the addition of exogenous ceramide to the embryos relieved the inhibition of Fumonisin B1. These results indicate that exposure of the maize embryos for 24 h to Fumonisin B1 allowed the mycotoxin to target ceramide synthase at the endoplasmic reticulum, eliciting an imbalance of endogenous sphingolipids. The latter disrupted membrane properties and inhibited the plasma membrane H-ATPase activity. Altogether, these results illustrate the mode of action of the pathogen and a plant defense strategy.
伏马菌素B1是由 产生的一种霉菌毒素,它会改变动物细胞膜的特性,并通过抑制神经酰胺合酶来抑制复杂鞘脂的合成。这项工作的目的是确定当将这种霉菌毒素添加到发芽的玉米胚中时,伏马菌素B1对植物质膜的影响。向胚中添加伏马菌素B1会降低质膜流动性,增加电解质渗漏,导致鞘氨醇增加7倍,质膜中的葡萄糖神经酰胺略有减少,而不影响植物鞘氨醇水平或脂肪酸组成。当胚在霉菌毒素存在的情况下发芽时,观察到质膜H-ATPase活性受到20%-30%的抑制。这种抑制仅与葡萄糖神经酰胺的减少有关,向胚中添加外源性神经酰胺可缓解伏马菌素B1的抑制作用。这些结果表明,玉米胚暴露于伏马菌素B1 24小时会使这种霉菌毒素靶向内质网中的神经酰胺合酶,引发内源性鞘脂的失衡。后者破坏了膜特性并抑制了质膜H-ATPase活性。总之,这些结果说明了病原体的作用方式和一种植物防御策略。