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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. [ABSTRACT FROM AUTHOR]

KP4 killer toxins are secreted proteins that inhibit cell growth and induce cell death in target organisms. In Fusarium graminearum, KP4-like (KP4L) proteins contribute to fungal virulence in wheat seedling rot and are expressed during Fusarium head blight development. However, fungal KP4L proteins are also hypothesized to support fungal antagonism by permeabilizing cell walls of competing fungi to enable penetration of toxic compounds. Here, we report the differential expression patterns of F. graminearum KP4L genes (Fgkp4l-1, -2, -3 and -4) in a competitive interaction, using Trichoderma gamsii as the antagonist. The results from dual cultures indicate that Fgkp4l-3 and Fgkp4l-4 could participate in the recognition at the distance of the antagonist, while all Fgkp4l genes were highly activated in the pathogen during the physical interaction of both fungi. Only Fgkp4l-4 was up-regulated during the interaction with T. gamsii in wheat spikes. This suggests the KP4L proteins could participate in supporting F. graminearum interspecific interactions, even in living plant tissues. The distribution of KP4L orthologous within the genus Fusarium revealed they are more represented in species with broad host-plant range than in host-specific species. Phylogeny inferred provides evidence that KP4L genes evolved through gene duplications, gene loss and sequence diversification in the genus Fusarium. [ABSTRACT FROM AUTHOR]

The pre-harvest biocontrol approach currently used includes laboratory inoculations using non-aflatoxigenic strains of Aspergillus flavus. This strategy effectively suppresses the indigenous aflatoxigenic strains and reduces aflatoxin accumulation in sweetcorn. The current in vitro study's main objective is to determine the diametric growth rates of both Aflatoxin (AF)+ and AF− strains and improve the understanding of competitive relationships among these strains in sweetcorn (Zea mays). Sweetcorn kernels inoculated with AF+ strains only, AF− strains only, and co-inoculated with AF+ + AF− strains were investigated for aflatoxin concentrations. The diametric growth results revealed that growth rates of AF− strains at 25 and 30 °C were much greater than AF+ strains, which was in line with previous studies. The in vitro findings showed that the AKR5− and AKL34− biocontrol strains effectively inhibited the colony propagation and subsequent AFB1 contamination (up to 79%) of AF+ strains. On the other hand, the AKR1− and AKL35− were least effective in reducing AFB1 contents only by 58% and 60%, respectively. There was a significant difference (p < 0.05) in the reduction of AFB1 contents achieved by AF− strains of A. flavus. The findings of the present study indicated the reduction in AFB1 with population expressions of AF+ strains by the AF− strains and supports the notion of competitive exclusion through vigorous development and propagation of the non-aflatoxigenic fungi. [ABSTRACT FROM AUTHOR]