Fusarium graminearum (FG) and Fusarium verticillioides (FV) co-occur in infected plants and plant residues. In maize ears, the growth of FV is stimulated while FG is suppressed. To elucidate the role of mycotoxins in these effects, we used FG mutants with disrupted synthesis of nivalenol (NIV) and deoxynivalenol (DON) and a FV mutant with disrupted synthesis of fumonisins to monitor fungal growth in mixed cultures in vitro and in co-infected plants by real-time PCR. In autoclaved grains as well as in maize ears, the growth of FV was stimulated by FG regardless of the production of DON or NIV by the latter, whereas the growth of FG was suppressed. In autoclaved grains, fumonisin-producing FV suppressed FG more strongly than a fumonisin-nonproducing strain, indicating that fumonisins act as interference competition agents. In co-infected maize ears, FG suppression was independent of fumonisin production by FV, likely due to heterogeneous infection and a lower level of fumonisins in planta. We conclude that (i) fumonisins are agents of interference competition of FV, and (ii) trichothecenes play no role in the interaction between FG and FV. We hypothesize the following: (i) In vitro, FG stimulates the FV growth by secreting hydrolases that mobilize nutrients. In planta, suppression of plant defense by FG may additionally play a role. (ii) The biological function of fumonisin production in planta is to protect kernels shed on the ground by accumulating protective metabolites before competitors become established. Therefore, to decipher the biological function of mycotoxins, the entire life history of mycotoxin producers must be considered.
Keywords: Fusarium; deoxynivalenol; fumonisins; fungal competition; mixed infection; nivalenol.