Bacillus velezensis EU07 suppresses Fusarium graminearum via transcriptomic reprogramming

Fusarium graminearum poses a major threat to global cereal production, necessitating sustainable control measures. This study elucidates the antagonistic mechanism of the biocontrol agent Bacillus velezensis EU07 against F. graminearum through combined transcriptomic and morphological analyses. Exposure to EU07 compromised fungal cellular integrity, causing severe hyphal distortion. RNA-seq profiling revealed that EU07 triggers a profound transcriptomic collapse rather than a standard stress response. Over 35% of the altered fungal transcriptome caused critical suppression, targeting essential metabolic hubs, secretome effectors, and master transcription factors to inhibit growth and loss of pathogenicity. In a compensatory defensive shift, the pathogen massively reallocated its transcriptional resources. This defence was characterised by a ~ 30-fold enrichment of transmembrane amino acid transporters for putative toxin efflux and an 80-fold enrichment of glutathione S-transferases to mitigate severe oxidative stress. Furthermore, EU07 suppressed core vulnerability nodes, including proline dehydrogenase (PRODH) and apolipophorin, disrupting the pathogen’s osmotic resilience and membrane integrity. Molecular docking analysis indicated that the Bacillus lipopeptide iturin A directly targets apolipophorin with high affinity (− 7.2 kcal/mol). Our findings indicated that B. velezensis EU07 overwhelms F. graminearum through simultaneous metabolic starvation and loss of virulence, revealing highly vulnerable fungal targets for next-generation RNAi-based biocontrol.

Highlights
- EU07 compromises fungal integrity and causes severe hyphal distortion
- The agent triggers a transcriptomic collapse, suppressing growth and virulence
- Iturin A targets apolipophorin, disrupting fungal membrane and resilience