|Authors: ||N. Al-Karablieh, A. Burse, H. Weingart, M. Ullrich|
The enterobacterium Erwinia amylovora causes fire blight on several plant species with economic importance such as apple and pear.
Infected plants produce phytoalexins, i.e., flavonoids, isoprenoids and alkaloids as biochemical defense mechanisms against pathogens.
A successful pathogen develops resistance mechanisms to combat the effect of these toxic compounds.
AcrAB-TolC multidrug efflux transporters which mediate resistance toward structurally unrelated compounds might confer tolerance to these phytoalexins.
To prove this hypothesis, single acrAB and tolC mutants and a double mutant (acrAB tolC) were constructed in E. amylovora strain 1189. The minimal inhibitory concentrations of different antimicrobial compounds and apple phytoalexins were determined for these mutants in comparison to the wild type.
Results indicated that the mutants were considerably more susceptible than the wild type suggesting that both, AcrAB and TolC, might interact in expelling toxic compounds in E. amylovora. All mutants and the wild type elicited hypersensitive reactions on tobacco plants demonstrating that the type III secretion system was not affected by mutations of acrAB or tolC. Virulence assays on apple plants showed that the virulence is impaired by mutation of acrAB or tolC. Analysis of secreted proteins is currently being conducted to investigate the role of TolC in protein secretion of E. amylovora.
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