Fusarium verticillioides produces fumonisins, which are mycotoxins inhibiting sphingolipid biosynthesis in humans, animals, and other eukaryotes. Fumonisins are presumed virulence factors of plant pathogens, but may also play a role in interactions between competing fungi. We observed higher resistance to added fumonisin B
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Fusarium verticillioides produces fumonisins, which are mycotoxins inhibiting sphingolipid biosynthesis in humans, animals, and other eukaryotes. Fumonisins are presumed virulence factors of plant pathogens, but may also play a role in interactions between competing fungi. We observed higher resistance to added fumonisin B
1 (FB
1) in fumonisin-producing
Fusarium verticillioides than in nonproducing
F. graminearum, and likewise between isolates of
Aspergillus and
Alternaria differing in production of sphinganine-analog toxins. It has been reported that in
F. verticillioides, ceramide synthase encoded in the fumonisin biosynthetic gene cluster is responsible for self-resistance. We reinvestigated the role of
FUM17 and
FUM18 by generating a double mutant strain in a
fum1 background. Nearly unchanged resistance to added FB
1 was observed compared to the parental
fum1 strain. A recently developed fumonisin-sensitive baker’s yeast strain allowed for the testing of candidate ceramide synthases by heterologous expression. The overexpression of the yeast
LAC1 gene, but not
LAG1, increased fumonisin resistance. High-level resistance was conferred by
FUM18, but not by
FUM17. Likewise, strong resistance to FB
1 was caused by overexpression of the presumed
F. verticillioides “housekeeping” ceramide synthases
CER1,
CER2, and
CER3, located outside the fumonisin cluster, indicating that
F. verticillioides possesses a redundant set of insensitive targets as a self-resistance mechanism.
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