Abstract
The catabolism of pectin from plant cell walls plays a crucial role in the virulence of the phytopathogen Dickeya dadantii. In particular, the timely expression of pel genes encoding major pectate lyases is essential to circumvent the plant defense systems and induce massive pectinolytic activity during the maceration phase. Previous studies identified the role of a positive feedback loop specific to the pectin-degradation pathway, whereas the precise signals controlling the dynamics of pectate lyase expression were unclear. Here, we show that the latter is controlled by a metabolic switch involving both glucose and pectin. We measured the HPLC concentration profiles of the key metabolites related to these two sources of carbon, cAMP and 2-keto-3-deoxygluconate, and developed a dynamic and quantitative model of the process integrating the associated regulators, cAMP receptor protein and KdgR. The model describes the regulatory events occurring at the promoters of two major pel genes, pelE and pelD. It highlights that their activity is controlled by a mechanism of carbon catabolite repression, which directly controls the virulence of D. dadantii. The model also shows that quantitative differences in the binding properties of common regulators at these two promoters resulted in a qualitatively different role of pelD and pelE in the metabolic switch, and also likely in conditions of infection, justifying their evolutionary conservation as separate genes in this species.
Highlights
The catabolism of pectin from plant cell walls plays a crucial role in the virulence of the phytopathogen Dickeya dadantii
Pectin degradation and KDG concentration peak occur before endo-pectate lyase (Pel) production boost The production of pectate lyases was monitored during D. dadantii growth in minimal medium supplemented with glucose or glucose+polygalacturonate (PGA), a simple form of pectin (Fig. 1A)
The latter acts as an inducer, boosting the production of enzymes by a factor of around 30 (Fig. 1B), which was previously attributed to the indirect activation of pel genes by the metabolite KDG resulting from PGA degradation (11, 12, 15): when KDG binds the regulator KdgR, it relieves transcriptional repression by the latter, triggering a positive feedback loop of pectin degradation (Fig. 2)
Summary
Shiny Martis B, Michel Droux, William Nasser, Sylvie Reverchon , and Sam Meyer* From the Laboratoire de Microbiologie, Adaptation et Pathogénie, Université de Lyon, INSA Lyon, Université Lyon 1, CNRS UMR 5240, Villeurbanne, France
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