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Title: Fumonisin B1 is necessary for corn seedling disease but is minimally translocated from roots to shoots

item Zimeri, Anne
item Williams, Lonnie
item Riley, Ronald
item Glenn, Anthony - Tony

Submitted to: Aflatoxin Elimination Workshop Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 10/16/2006
Publication Date: 10/16/2006
Citation: Zimeri, A.M., Williams, L.D., Riley, R.T., Glenn, A.E. 2006. Fumonisin B1 is necessary for corn seedling disease but is minimally translocated from roots to shoots. Aflatoxin Elimination Workshop Proceedings. October 16 - 18, 2006. Fort Worth, Texas.

Interpretive Summary: Abstract - no summary needed.

Technical Abstract: Fusarium verticillioides, the causative agent of corn seedling blight and ear rot, produces the mycotoxin fumonisin B1 (FB1). The toxicity of FB1 is due to its inhibition of ceramide synthase, a key enzyme necessary for sphingolipid metabolism. Such inhibition occurs in both animals and plants. For example, FB1 is known to inhibit ceramide synthase in tomato, causing and increase in free sphinganine and phytosphingosine, which are ceramide precursors. We recently reported that roots of corn seedlings inoculated with F. verticillioides had elevated free sphinganine and phytosphingosine as well as their respective 1-phosphates. Thus, FB1 produced by F. verticillioides can inhibit ceramide synthase in corn. Additionally, FB1 production by F. verticillioides strains was tightly linked to their pathogenicity. FB1-producing strains caused necrotic leaf lesions, developmental abnormalities, severe stunting, and even death of "Silver Queen" seedlings. Non-producing strains were able to systemically infect seedlings but did not cause the foliar disease symptoms. Exposing seedlings to FB1 in the absence of F. verticillioides caused some leaf lesions, though the full spectrum of symptoms was not as severe as when the fungus was present. Corn lines were assessed for their sensitivity to FB1, and B73, FR1064, CG1, Mo17, and CQ201 were unable to germinate on media containing 100 µM FB1. "Silver Queen" had a lower germination rate (12%) and stunted growth (44.1% of the control for root weight, 58.3% of the control for shoot weight, and 75% of the control for shoot height). Of the lines evaluated, only W23 was truly insensitive with 100% germination and equal or better growth compared to control plants (98.8% of the control for root weight; 128.6% of the control for shoot weight; and 124% of the control for shoot height). Plants were also exposed to extracts of fungal cultures grown on autoclaved corn kernels. Extracts containing FB1 exhibited the full suite of symptoms as occurs on plants infected with FB1 producing strains. In addition, we found that aerial portions of plants subjected to this treatment contained FB1 (0.0044 ppm), suggesting the metabolite was taken up by roots and translocated by the plant vasculature. However, active uptake and translocation of FB1 into leaf tissue was minimal (60-90 fold less in leaves than in roots). The insensitivity of W23 to FB1 compared to sensitive lines B73 and "Silver Queen" was not due to differential translocation and accumulation of FB1 in leaf tissues since they all passively accumulated FB1 (1.3 to 2.6 ppm) in a detached leaf assay. Accumulation of fumonisin in kernels via translocation was assessed by injecting fungal culture extracts containing FB1 into stalks of "Tom Thumb" below developing ears prior to pollination. Resulting kernels were collected and sampled for fungal infection as well as for FB1 contamination. Translocation and accumulation of the injected FB1 was not supported. However, the injected fungal extracts appeared to confer resistance because the extract treatments had less F. verticillioides infection and only 0.7 ppm total fumonisin contamination compared to 3.1 ppm in the control kernels. Thus, while FB1 production by F. verticillioides was necessary for development of foliar disease symptoms on seedlings, the mycotoxin apparently was not translocated or accumulated to high levels in the leaves, suggesting the disease development may not involve localized ceramide synthase inhibition in the leaves but may result from another mobile signal or pathway. Furthermore, the apparent lack of FB1 accumulation in the kernels via translocation is encouraging from the standpoint of control strategies, and additional studies are planned to more closely evaluate our initial data on suppression of F. verticillioides infection and FB1 contamination of kernels by fun