After studying the wild cell behavior, one of our solutions to turn off its virulence was to genetically modify Erwinia amylovora. We introduced a gene that codifies to an AHL degrading enzyme, AHL-lactonase (aiiA). In bacterial pathogens, this enzyme disrupts bacterial quorum sensing, consequently inhibiting the production of pathogenesis factors.

In this modified bacteria, the aiiA gene (green rectangle) codifies to our antidote protein (green oval) in an unregulated manner. After some time, the protein production will reach a constant production big enough to act on the quorum sensing regulation. With a constitutive aiiA expression, we expect a complete and uninterrupted inhibition of the AHLs activity by hydrolyzing them and varying the lengths of their acyl chains, modifying their conformational structure. Therefore its autoregulation will be unable to be completed, resulting in no more AHL production.

To model the behavior of this gene inside Erwinia amylovora, we first came to several assumptions discussed below.


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