Optimization of Fusarium graminearum conidia for the application of virus-induced hypovirulence in the field

• Applicant: Privatdozentin Dr. Cornelia Heinze
• Subject Area: Plant Breeding and Plant Pathology
• Term: since 2025
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 562738208

Fusarium graminearum is the causal agent of Fusarium head blight (FHB), which is a devastating worldwide disease of several cereals, including wheat and maize. Today, the use of chemical fungicides is the major approach for the control of FHB-epidemics, though its efficiency is hampered by a critical timepoint of application. Hence, alternative strategies for effective control measures have to be developed and implemented. One innovative strategy is the use of virus-mediated hypovirulence, which means the use of mycoviruses that reduce the virulence of their fungal hosts. One of the viruses that causes hypovirulence in F. graminearum is the Fusarium graminearum virus China 9 (FgV-ch9). With this, the development and implementation of an FHB biocontrol system seem feasible. The application of hypovirulent fungal strains for the treatment of annual crops is challenging, but the use of virus-infected spores may be an option. However, we know that the conidia only partially germinate into hypovirulent mycelium, depending on the viral load of the mycelium from which they were generated. The mechanism of virus transfer into conidia is not known, but it is assumed that viruses must be present in the conidiophores in a sufficient number. Preliminary studies indicate that RNAi and the fungal SOFT (SO) protein are involved in the FgV-ch9 distribution in the mycelium and consequently that conidiophores contain a variable amount of virus, which leads to only partially immigration into conidia. To increase the percentage of FgV-ch9-infected conidia, RNAi-deficient and SO-overexpressing mutants will be generated. Another protein could be interesting in this context. SO and the mitogen-activated protein kinase 2 (MAK2) interact to enable anastomosis formation. When a MAK2 overexpression behaves similarly to a SO-overexpression, a simultaneous overexpression of both may lead to the highest percentage of virus-infected conidia. To verify our results at the cellular level, labeling of virus particles is necessary. In preliminary studies, we were able to express a reportergen with the help of an artificial viral segment. For its use to label specifically virus particles for their localization and tracking their migration, the system must be adapted and optimized. We hope that the results obtained by the submitted project will give us more insights into the virus migration in fungi and bring us a step towards the practical application of virus-mediated hypovirulence in the field.

• DFG Programme: Research Grants