Brachypodium distachyon as a genetic model pathosystem to study resistance against fungal pathogens of small grain cereals
ABSTRACT Fusarium head blight (FHB) and other Fusarium diseases of wheat and other small-grain cereals cause yield reduction and grain contamination with harmful mycotoxins, mainly deoxynivalenol (DON). Little is known about the mechanistic basis of resistance to Fusarium in cereals due to the large, polyploid and unsequenced genome of wheat. Host ethylene (ET) signalling was previously shown to be a factor of susceptibility to FHB. Chapter 2 uses wheat EMS mutant lines characterized for altered senescence to test for a relationship between ET-sensitivity, senescence and resistance to FHB. Candidate mutant lines displaying high level of resistance to FHB were identified and resistance was associated with delayed senescence, reduced ET-sensitivity, or developmental delay. Brachypodium distachyon (Bd) has the potential to serve as a model pathosystem relevant to small-grain cereals. Chapter 3 provides evidence of compatibility between Bd and the main causal agents of FHB and shows that symptom development mirrors closely that in wheat. Natural variation in disease resistance exists among Bd accessions and a novel route for initial infection is suggested. Bd is also compatible with other important pathogens of small-grain cereals causing ramularia, eyespot and take-all diseases. In Chapter 4, a preliminary study of Bd T-DNA mutant lines altered in phytohormone biosynthesis or response investigates alteration of Fusarium resistance. Mutation of the main brassinosteroid (BR) receptor (BRI1) was characterized and validated. Other mutants defective in auxin or ET responsiveness and jasmonic acid (JA) biosynthesis were investigated. Results suggest that JA and BRI1 promote disease susceptibility. Finally, Chapter 5 uses a chemical and genetic approach to investigate the mechanisms of DON phytotoxicity using the Bd root system. Effects induced by the mycotoxin are compared with BRs, inhibitors of protein synthesis and compounds altering BR biosynthesis or signalling. Results suggest that DON may disrupt host BR homeostasis to promote disease susceptibility.
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