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Flavonoid biosynthesis and degradation play a role in early defence responses of bilberry (Vaccinium myrtillus) against biotic stress

Bilberry (Vaccinium myrtillus) represents one of the richest flavonoid sources among plants. Flavonoids play variable, species-dependent roles in plant defences. In bilberry, flavonoid metabolism is activated in response to solar radiation but not against mechanical injury. In this paper, the defenc...

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Bibliographic Details
Published in:European journal of plant pathology 2009-12, Vol.125 (4), p.629-640
Main Authors: Koskimäki, Janne J, Hokkanen, Juho, Jaakola, Laura, Suorsa, Marja, Tolonen, Ari, Mattila, Sampo, Pirttilä, Anna Maria, Hohtola, Anja
Format: Article
Language:English
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Summary:Bilberry (Vaccinium myrtillus) represents one of the richest flavonoid sources among plants. Flavonoids play variable, species-dependent roles in plant defences. In bilberry, flavonoid metabolism is activated in response to solar radiation but not against mechanical injury. In this paper, the defence reaction and biosynthesis of phenolic compounds of bilberry was studied after infection by a fungal endophyte (Paraphaeosphaeria sp.) and a pathogen (Botrytis cinerea). The defence response of bilberry was faster against the endophyte than the pathogen. All flavonoid biosynthesis genes tested were activated by each infection. Biosynthesis and accumulation of phenolic acids, flavan-3-ols and oligomeric proanthocyanidins were clearly elevated in both infected samples. Infection by the pathogen promoted specifically accumulation of epigallocatechin, quercetin-3-glucoside, quercetin-3-O-α-rhamnoside, quercetin-3-O-(4”-HMG)-R-rhamnoside, chlorogenic acid and coumaroyl quinic acid. The endophyte-infected plants had a higher content of quercetin-3-glucuronide and coumaroyl iridoid. Therefore, accumulation of individual phenolic compounds could be specific for each infection. Quantity of insoluble proanthocyanidins was the highest in control plants, suggesting that they might act as storage compounds and become activated by degradation upon infection.
ISSN:0929-1873
1573-8469
DOI:10.1007/s10658-009-9511-6