Our group studies molecular mechanism of Type III secretion systems.
In our ongoing research we are using genetics to introduce different fluorescence and epitope tags in genes encoding the different T3SS components, regulators and secretion substrates to facilitate studies of the kinetics and mechanism of T3SS mediated targeting of virulence effectors into host cells using advance fluorescence and electron microscopy.
T3SSs are organized into supra-molecular structures known as needle complexes and this structure, which is believed to be common to all T3SSs, resembles a syringe with a base structure and a needle-like protrusion extending from the surface of the pathogen. The entire needle complex is traversed by a fine, hollow tube that may allow passage of effector proteins across the bacterial cell envelope.
Due to the suggestive similarities between the needle complex and a syringe, it has been generally accepted that the effectors travel directly through the needle complex from the bacterial cytosol into the eukaryotic target cell through a pore induced by the secreted translocaters. Recent studies that have shown that both the effectors and translocaters actually are present on the surface of the bacterial cell prior to cell contact and that purified effectors added externally to an infected can be targeted into the host cell. Based on this an alternative working model for translocation has been suggested.