Fusarium head blight epidemics of wheat and barley cause heavy economic losses to farmers due to yield decreases and production of
mycotoxin that renders the grain useless for flour and malt products. No highly resistant cultivars are available at present. Hyphae of germinating fungal spores use different paths of
infection: After germination at the extruded tip of an ovary, the hyphae travel along the epicarp in the space between the lemma and palea.
Infection of the developing kernel proceeds through the epicarp, successively destroying the layers of the fruit coat and finally the
starch and
protein accumulating endosperm. Hyphae reaching the rachis proceed to apically located developing kernels. Using a constitutively green fluorescence
protein-expressing Fusarium wild-type strain, and its knockout mutant, preventing
trichothecene synthesis, we demonstrate that
trichothecenes are not a
virulence factor during
infection through the fruit coat. In the absence of
trichothecenes, the fungus is blocked by the development of heavy cell wall thickenings in the rachis node of Nandu wheat, a defense inhibited by the
mycotoxin. In barley hyphae of both wild-type and the
trichothecene knockout mutant, are inhibited at the rachis node and rachilla, limiting
infection of adjacent florets through the phloem and along the surface of the rachis. Effective resistance to Fusarium head blight requires expression of genes that combat these different pathways of
infection.