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Modeling the onset of virulence in a pectinolytic bacterium
Jacques-A Sepulchre1, Sylvie Reverchon, William Nasser
1Institut Non Linéaire de Nice, UNSA-CNRS, 1361 Route des Lucioles, 06560 Valbonne Sophia Antipolis, France. jacques-alexandre.sepulchre@inln.cnrs.fr
Abstract:
Building up from experimental knowledge of the regulatory network of the pel genes in the bacteria E. chrysanthemi, we propose for the first time a qualitative modeling of the infectious transition of this bacteria when it is hosted in a plant. We show that this infectious transition can be understood as the excitable dynamics of a metabolico-genetic network. Our mathematical model can account for the main phases which are observed in the onset of the pathogenecity by Erwinia chrysanthemi, namely the silent, latent and virulent stages. Like in many infectious agents, the silent state corresponds to the growth phase of the bacteria, where they multiply without significantly producing molecules which could trigger a counter attack of the invaded host. The latent stage is characterized by a moderate but unequivocal expression of the virulence gene, waiting for a number of conditions which have to fulfill in order to trigger a fully developed infection. In the virulent state the bacteria synthesize a massive production of virulence factors including pectate lyases (Pel) which favor the invasion of the host plant tissues. Our model is able to show cases of transitions from the silent to the virulent stages of the infection, using the method of the piecewise-affine (PA) differential equations and its implementation in the genetic network analyser software (GNA). The obtained qualitative dynamics of the models are consistent with the current experimental data about this system. Moreover it can be interpreted with respect to the relatively complex structure of the binding sites of pel. From the biological point of view, our simulations validate the picture that the promoter of pel has evolved to form a security device preventing a hastened expression of these virulent genes. This first modeling of the regulation of pel genes opens the way to new confrontations between theoretical ideas with experiments and possible strategies to fight the soft-rot disease of plants.
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