Tracking of Tobacco Mosaic Virus in Taxonomically Different Plant Fungi

Summary

Scientists discovered that a common plant virus (tobacco mosaic virus) can infect and multiply inside certain fungal pathogens that harm crops. When the virus enters these fungi, the fungi activate their natural defense system to fight back. Interestingly, the virus doesn’t make the fungi more or less dangerous to plants. This discovery opens new possibilities for controlling harmful fungi using viruses as biological tools.

Background

Plant viruses have traditionally been considered pathogens restricted to plant hosts, but recent studies demonstrate that some plant viruses can infect and replicate in filamentous fungi and oomycetes, suggesting broader host ranges and more complex ecological interactions. This study investigates cross-kingdom viral transmission and interactions between plant viruses and fungal pathogens.

Objective

To investigate the ability of Tobacco mosaic virus (TMV) to replicate in four major phytopathogenic fungi from different taxonomic groups: Botrytis cinerea, Fusarium oxysporum f. sp. lycopersici, Verticillium dahliae, and Monilinia fructicola. The study also aimed to explore the role of RNA interference (RNAi) in virus-fungus interactions and assess TMV’s suitability as a tool for fungal functional genomics.

Results

TMV successfully entered and replicated in B. cinerea and V. dahliae mycelia but not in F. oxysporum or M. fructicola. Both susceptible fungi showed strong induction of RNAi pathway genes (DCL1 and AGO1), indicating antiviral responses. Despite viral replication and RNAi activation, the pathogenicity of infected fungi on their respective host plants remained unaffected.

Conclusion

The findings reinforce the recognition of cross-kingdom virus transmission and interactions with crucial implications for pathogen ecology and viral evolution. TMV-based vectors demonstrate potential as tools for functional genomic studies in fungi. Understanding these virus-fungus interactions provides insights into RNAi silencing mechanisms and may inform new biocontrol strategies against fungal pathogens.
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