The trichothecene mycotoxin deoxynivalenol facilitates cell-to-cell invasion during wheat-tissue colonisation by Fusarium graminearum

Fusarium Head Blight (FHB) disease on small grain cereals is primarily caused by the ascomycete fungal pathogen Fusarium graminearum. Infection of floral spike tissues is characterised by the biosynthesis and secretion of potent trichothecene mycotoxins, of which deoxynivalenol (DON) is widely reported due to its negative impacts on grain quality and consumer safety. The TRI5 gene encodes an essential enzyme in the DON biosynthesis pathway and the single gene deletion mutant,{Delta} Tri5, is widely reported to restrict disease progression to the inoculated spikelet. In this study, we present novel bioimaging evidence revealing that DON facilitates the traversal of the cell wall through plasmodesmata, a process essential for successful colonisation of host tissue. Chemical complementation of{Delta} Tri5 did not restore macro- or microscopic phenotypes, indicating that DON secretion is tightly regulated both spatially and temporally. A comparative qualitative and quantitative morphological cellular analysis revealed infections had no impact on plant cell wall thickness. Immuno- labelling of callose at plasmodesmata during infection indicates that DON can increase deposits when applied exogenously, but is reduced when F. graminearum hyphae are present. This study highlights the complexity of the inter-connected roles of mycotoxin production, cell wall architecture and plasmodesmata in this highly specialised interaction.