Induced tolerance of 'Sclerotinia sclerotiorum' to isothiocyanates and toxic volatiles from 'Brassica' species

Author(s)
Rahmanpour, Siamak
Backhouse, David
Nonhebel, Heather
Publication Date
2009
Abstract
The response of 'Sclerotinia sclerotiorum' , the causal agent of stem rot of oilseed rape ('Brassica napus'), to toxic volatiles produced by the glucosinolate-myrosinase system was studied. Mycelium plugs were exposed to inoculated leaf discs of oilseed rape cultivars and two related species, black mustard ('Brassica nigra') and white mustard ('Sinapis alba'). Growth of exposed colonies was inhibited by more than 87% compared with controls. Despite inhibition of exposed fungal colonies, the fungus continued to grow in infected tissue. Repeated exposure of the fungus to hydrated mustard powder (which contains both glucosinolates and myrosinase) or synthetic isothiocyanates (ITCs) resulted in growth inhibition decreasing from initial levels of up to 80% to insignificant levels after 2–3 days, suggesting that 'S. sclerotiorum' has the ability to adapt to volatiles during the infection progress. This adaptation was studied by investigating induction of glutathione S-transferase-like genes identified from the 'S. sclerotiorum' genome. Three genes, with locus numbers SS1G_07195.1, SS1G_01918.1 and SS1G_10295.1, appeared to be up-regulated following exposure of 'S. sclerotiorum' to mustard powder or allyl ITC. A fourth gene, SS1G_07319.1, appeared to be down-regulated. In addition, glutathione S-transferase catalytic activity in crude mycelium extracts was doubled following 48 h of exposure to mustard powder volatiles. This adaptation could allow 'S. sclerotiorum' to parasitize tissues of 'Brassica' species despite the production of toxic metabolites.
Citation
Plant Pathology, 58(3), p. 479-486
ISSN
1365-3059
0032-0862
Link
Language
en
Publisher
Wiley-Blackwell Publishing Ltd
Title
Induced tolerance of 'Sclerotinia sclerotiorum' to isothiocyanates and toxic volatiles from 'Brassica' species
Type of document
Journal Article
Entity Type
Publication

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