Location: Toxicology and Mycotoxin Research
Title: Disruption of ceramide biosynthesis and accumulation of sphingoid bases and sphingoid base 1-phosphates: A mechanism for Fusarium verticillioides effects in maize-seedling disease. Authors
|Williams, Lonnie - BURDOCK GROUP,VERO BCH/FL|
|Smith, Mary - ENV HLTH SCI/UGA,ATHENS|
Submitted to: Multicrop Aflatoxin and Fumonisin Elimination and Fungal Genomics Workshop-The Peanut Foundation
Publication Type: Proceedings
Publication Acceptance Date: October 24, 2007
Publication Date: October 22, 2007
Citation: Williams, L.D., Zitomer, N.C., Glenn, A.E., Bacon, C.W., Smith, M.A., Riley, R.T. 2007. Disruption of ceramide biosynthesis and accumulation of sphingoid bases and sphingoid base 1-phosphates: A mechanism for Fusarium verticillioides effects in maize-seedling disease.. Multicrop Aflatoxin and Fumonisin Elimination and Fungal Genomics Workshop-The Peanut Foundation. October 22 - 24, 2007.Atlanta, GA. Interpretive Summary: Abstract - no summary required.
Technical Abstract: In sweet corn at the seedling and seed maturation stages, Fusarium can be a serious field problem. The fungus Fusarium verticillioides infects maize and produces fumonisins, inhibitors of ceramide synthase. To determine the role of fumonisins in maize seedling disease, seeds were inoculated with fumonisin producing or non-producing strains of F. verticillioides. Silver Queen (SQ) seedlings grown from seeds inoculated with the producing strains had detectable fumonisins in roots and soils, and sphingoid bases and sphingoid base 1-phosphates were elevated in roots. Leaf lesions and abnormal leaf developmental were only observed with producing strains and while non-producing strains of F. verticillioides caused reduced root and stalk growth the effect on growth was greatest with producing strains. Leaf lesion incidence and severity of effects on root and stalk growth were significantly correlated with fumonisin in roots and the extent of disruption of sphingolipid metabolism in roots. In a subsequent study with the fumonisin producing strain MRC826, seedlings grown from inoculated seeds were harvested on days 7, 14 and 21. Reduced growth of aerial plant parts and roots were seen in seedling as early as day 7, however, leaf lesions were not apparent until day 14. Fumonisins were detected in the roots of seedlings and was maximal on day 14. There were significant increases in free sphingoid bases on day 7 which were maximal on day 14. There were also significant increases in free sphingoid base 1-phosphates on day 7. However, the level of free sphinganine 1-phosphate (Sa 1-P) decreased significantly after day 7. These results suggest a time-dependent adaptive response to disrupted sphingolipid metabolism after prolonged fumonisin exposure. FB1 was also detected in leaf tissues grown from inoculated seeds. Surprisingly, FB1 was preferentially accumulated in leaves of SQ and W23 over FB2 and FB3. The levels of accumulation of FB1 in the 1st leaf paralleled the known susceptibility of the two lines to F. verticillioides induced leaf lesions and the levels of FB1 in all leafs of the susceptible sweet maize SQ variety were significantly (p<0.001) greater than in the resistant dent maize variety W23. Disruption of sphingolipid metabolism as measured by accumulation of phytosphingosine (Pso), sphinganine (Sa), Pso 1-phosphate (Pso 1-P), and Sa 1-P, was easily demonstrated in the SQ line. For all leaves, the MRC826 treated plants had significantly elevated sphingoid bases and their 1-phosphates, and the levels were not significantly different between leaves. This was not the case in the W23 line where significant increases occurred only in the 2nd leaf and 3rd leaf. In all cases the elevations in W23 were significantly less than the elevations observed in SQ. The results support the hypothesis that fumonisin is necessary and sufficient to produce the full spectrum of symptoms indicative of F. verticillioides-induced maize seedling disease in SQ and that the mechanism of action involves both the ability to accumulate FB1 and its disruption of sphingolipid metabolism.