Abstract
AbstractTake-all disease, caused by the soil-borne ascomycete fungusGaeumannomyces tritici, is one of the most important root diseases of wheat in the UK and worldwide. The fungus invades the roots and destroys the vascular tissue, hindering the uptake of water and nutrients from the soil. Closely related non-pathogenic species in theMagnaporthaceaefamily, such asGaeumannomyces hyphopodioides, occur naturally in arable and grassland soils and have previously been reported to reduce take-all disease in field studies. Here, we characterise the different infection structures produced byG. triticiandG. hyphopodioidesand suggest an alternative role for previously described “sub-epidermal vesicles” (SEVs). We show that direct interaction between the two species is unlikely to play a significant role in take-all control, and instead demonstrate that take-all control is achieved via local host changes in response to priorG. hyphopodioidesroot colonisation. RNA sequencing revealed extensive host transcriptional reprogramming inG. hyphopodioidescolonised tissues, characterised by a striking downregulation of key cell-wall related genes, including cellulose synthase (CESA), and xyloglucan endotransglucosylase/hydrolase (XTH) genes. In the absence of take-all resistant wheat cultivars and avirulentG. triticistrains, studying closely relatedG. hyphopodioidesprovides a much-needed avenue to elucidate take-all resistance mechanisms in wheat.
Publisher
Cold Spring Harbor Laboratory
Cited by
2 articles.
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