Abstract:
Effector proteins of gram-negative bacteria are translocated into the host cytosol via the type-III-secretion system to suppress host innate immune reactions, which are activated after perception of specific pathogenic surface structures. HrpZ1, an effector protein of phytopathogenic pseudomonads, is secreted into the plant apoplast via the type-III-pathway and induces plant innate immune reactions, that, however, are not caused by the ion pore formation ability of the protein. These immune reactions rely on the immunostimulatory activity of the HrpZ1-protein, similar to classical PAMPs, and are probably mediated by a plant plasma membrane-localized receptor. Due to the homooligomerization ability, the characteristic and specific conformational change after transition from hydrophillic into lipophillic, membrane-mimicking environments and, additionally, the pore formation ability in synthetic and natural lipid bilayers it is conceivable, that HrpZ1 contributes to pore formation in the plant plasma membrane during infection to support, most likely, the injection of type-III effector proteins into the host cytosol.