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• W2169536239 abstract "Plant primary energy metabolism is profoundly reorganized under biotic stress conditions and there is increasing evidence for a role for the fermentative pathway in biotic interactions. However, the mechanisms regulating metabolic reprogramming are not well understood despite its critical function in the biotic stress response. Here the function of alcohol dehydrogenase (ADH) in the interaction of barley with the parasitic fungus Blumeria graminis f.sp. hordei (Bgh) is addressed. Challenge of susceptible barley leaves with Bgh resulted in transcriptional activation of HvADH1 and an induction of ADH enzyme activity starting 24 h after infection and reaching a clear-cut effect 4 d after infection. This increase in ADH enzyme activity was not observed in the resistant near-isogenic mlo5 line. Moreover, an induction of ADH enzyme activity by Bgh was enhanced in the presence of sucrose in hydroponically grown seedlings. Transient knock-down or overexpression of HvADH1 in barley epidermal cells mediated a decrease or increase in the penetration success of Bgh, respectively. Inhibition of ADH activity by pyrazole resulted in a delay in symptoms. The pyrazole effect could be overcome by adding glucose to the incubation medium, pinpointing a nutritional effect of ADH in the barley-Bgh interaction. Taken together, misexpression of pathogen-inducible HvADH1 or variation of ADH activity modulates the pathogen response of barley to the biotrophic fungal parasite Bgh. In this way, ADH knock-down/inhibition results in reduced fungal success. The possibility is discussed that ADH activity supports biotrophy by maintaining glycolytic metabolism in pathogen-stressed barley." @default.
• W2169536239 created "2016-06-24" @default.
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• W2169536239 date "2011-02-21" @default.
• W2169536239 modified "2023-10-16" @default.
• W2169536239 title "Alcohol dehydrogenase 1 of barley modulates susceptibility to the parasitic fungus Blumeria graminis f.sp. hordei" @default.
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• W2169536239 doi "https://doi.org/10.1093/jxb/err017" @default.
• W2169536239 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3130169" @default.
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