Technical Abstract: Fusarium verticilliodes, the causative agent of ear rot in corn, can produce the mycotoxin fumonisin B1 (FB1). FB1 inhibits a key eukaryotic enzyme necessary for sphingolipid metabolism, ceramide synthase. Such inhibition causes a number of species-specific animal diseases and may contribute to cancer and perhaps neural tube defects in humans. We previously showed FB1 was also a phytotoxin affecting corn development via disruption of sphingolipid metabolism. Yet, some corn lines infected with Fusarium contain significant FB1 levels in the kernels despite not always exhibiting phenotypic signs of disease. We hypothesize that FB1 phytotoxicity is ancestral in com and that breeding programs may have selected for asymptomatic endophytic associations in which visible disease such as ear rot is diminished, yet FB1 accumulation may still occur to significant levels. To test this hypothesis, we have collected physiological data for both root and aerial tissues of various corn lines exposed to FB1. We are also evaluating lines of Tripsacum and teosinte. Data thus far support the hypothesis that sensitivity to FB1 is ancestral among corn and that resistance to the toxicity of FB1 is the derived characteristic. In addition, uninfected sensitive and resistant lines of corn both exhibited stimulated growth in aerial tissues in response to low levels of FB1 (1 microgram/mL), while higher FB1 levels (>5 microgram/mL) severely inhibited growth of both above- and below-ground tissues of sensitive lines. Seedlings were analyzed for FB1 accumulation in leaves using LCMS, but the toxin was not detected. We are currently using LCMS to determine whether other molecules in the sphingolipid pathway, upstream of ceramide synthase, are increased in aboveground tissues.