3 years ago

Contribution of the β-glucosidase BglC to the Onset of the Pathogenic Lifestyle of Streptomyces scabies

Elodie Tenconi, Rosemary Loria, Isolde M. Francis, Bart Devreese, Sören Planckaert, Jennifer Riley, Benoit Deflandre, Loïc Martinet, Sébastien Rigali, Pierre Tocquin, Samuel Jourdan
Common scab disease on root and tuber plants is caused by Streptomyces scabies and related species which use the cellulose synthase inhibitor thaxtomin A as the main phytotoxin. Thaxtomin production is primarily triggered by the import of cello-oligosaccharides. Once inside the cell, the fate of the cello-oligosaccharides is dichotomized into i) fueling glycolysis with glucose for the saprophytic lifestyle through the action of β-glucosidase(s) (BG), and ii) eliciting the pathogenic lifestyle by inhibiting the CebR-mediated transcriptional repression of thaxtomin biosynthetic genes. Here we investigated the role of scab57721 encoding a putative BG (BglC) in the onset of the pathogenicity of S. scabies. Enzymatic assays showed that BglC was able to release glucose from cellobiose, cellotriose and all other cello-oligosaccharides tested. Its inactivation resulted in a phenotype opposite to what was expected as we monitored reduced production of thaxtomin when the mutant was cultivated on media containing cello-oligosaccharides as unique carbon source. This unexpected phenotype could be attributed to the highly increased activity of alternative intracellular BGs, probably as a compensation of bglC inactivation, which then prevented cellobiose and cellotriose accumulation to reduce the activity of CebR. In contrast, when the bglC null mutant was cultivated on media devoid of cello-oligosaccharides it instead constitutively produced thaxtomin. This observed hypervirulent phenotype does not fit with the proposed model of the cello-oligosaccharide-mediated induction of thaxtomin production and suggests that the role of BglC in the route to the pathogenic lifestyle of S. scabies is more complex than currently presented. This article is protected by copyright. All rights reserved.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/mpp.12631

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