Effects of Disruption of Five FUM Genes on Fumonisin Biosynthesis and Pathogenicity in Fusarium proliferatum

Abstract

The mycotoxin fumonisin is known to be harmful to humans and animals, and thus it is desirable to reduce fumonisin content in crop products. We explored the functions of several genes that function in fumonisin biosynthesis (<i>FUM1</i>, <i>FUM6</i>, <i>FUM8</i>, <i>FUM19</i>, and <i>FUM21</i>) in <i>Fusarium proliferatum</i> and found that deletion of <i>FUM1</i>, <i>FUM6</i>, <i>FUM8</i>, or <i>FUM21</i> results in a severe reduction in fumonisin biosynthesis, while loss of <i>FUM19</i> does not. In addition, fumonisin-deficient strains display significantly decreased pathogenicity. Co-cultivation of the Δ<i>FUM1</i>, Δ<i>FUM6</i>, Δ<i>FUM8</i>, and Δ<i>FUM19</i> mutants restores fumonisin synthesis. However, co-cultivation was unable to restore fumonisin synthesis in the Δ<i>FUM21</i> strain. The relative expression levels of three key <i>FUM</i> genes (<i>FUM1</i>, <i>FUM6</i>, and <i>FUM8</i>) differed significantly in each mutant strain; notably, the expression levels of these three genes were significantly down-regulated in the Δ<i>FUM21</i> strain. Taken together, our results demonstrate that <i>FUM1</i>, <i>FUM6</i>, <i>FUM8</i>, and <i>FUM21</i> are essential for fumonisin synthesis, and <i>FUM19</i> is non-essential. Partial mutants lost the ability to synthesize fumonisin, the co-culture of the mutants was able to restore fumonisin biosynthesis. While the pathogenicity of <i>F. proliferatum</i> is affected by many factors, inhibition of the synthesis of the mycotoxin fumonisin will weaken the pathogenicity of rice spikelet rot disease (RSRD).