Understanding the mechanisms of host-tissue colonisation by Fusarium graminearum

Abstract

Fusarium graminearum is an ascomycete fungal pathogen that infects small grain cereals and leads to large reductions in yields due to reduced grain wights and contamination of developing grain with potent mycotoxins. Some of these are trichothecene mycotoxins, and are required for virulence when infecting wheat. Their potent toxicity to eukaryotic ribosomes dampens broad-spectrum protein translation and facilitates host-tissue colonisation by invasive hyphae. This thesis explores the intracellular role of deoxynivalenol (DON), one of the most prolific mycotoxins, and its role in wheat spikelet infection with respect to the crossing of wheat cell walls through plasmodesmatal pit fields.

Single gene deletion of an essential enzyme for the biosynthesis of trichothecene mycotoxins, ΔTri5, leads to restriction of infection to inoculated wheat spikelets by failing to prevent the deposition of callose, a β-1,3-glucan polymer, at plasmodesmata during biotic and abiotic stress to symplastically isolate cells. In the wild-type (WT) compatible interaction, invasive hyphae break through plasmodesmatal pit fields to facilitate host-tissue colonisation. This led to studies exploring PAMP-triggered immunity in the absence of DON in wheat floral tissues and the role of cell wall components as resistance or susceptibility factors to hyphal colonisation. On the other side of the interaction, studies contained within this thesis have identified a Fusarium graminearum-secreted Glycoside Hydrolase family 81 (GH81) enzyme that is predicted to hydrolyse callose deposited at plasmodesmatal pit fields during infection. Overall, this thesis both advances our understanding of the use of plasmodesmatal pit fields by F. graminearum during host-tissue colonisation in wheat spikes and opens new avenues for exploration.