Fusarium graminearum is a serious fungal pathogen of small grain cereals and the causal agent of Fusarium Head Blight/Head Scab disease. Infection occurs at anthesis and during grain development contaminates the grain with various trichothecene mycotoxins. Of these, deoxynivalenol (DON) is particularly harmful to both livestock and humans, designating grain unsuitable for ingestion. TRI5 encodes an enzyme that catalyses the biosynthesis of DON and disruption of this gene eliminates trichothecene synthesis. The single gene deletion mutant, ΔTri5, does not produce DON and is unable to colonise beyond the rachis node of inoculated wheat spikelets. However, the role of DON as a virulence factor is specific to the wheat floral interaction. Prior to this study, a cellular restructuring role for DON had not been considered. Through microscopic analysis, we report that in the absence of DON, F. graminearum is inhibited in its ability to traverse plasmodesmata (PD). PD have evolved defence mechanisms against fungal, bacterial and viral pathogens which includes modifying the surrounding cell wall. This study poses new hypotheses surrounding the working disease model for F. graminearum, creating new questions encompassing the role of the cell wall structure in disease resistance and the role(s) PD have in modifying host-fungal pathogen interaction outcomes.