Salmonella injects effector proteins into host cells through the injectisome, a virulence-associated type-III secretion system (vT3SS). We study which cells express it and how its substrates reach the export apparatus.
During the initial phase of infection, Salmonella Typhimurium uses flagella to reach the intestinal epithelium. It then uses the vT3SS encoded on Salmonella pathogenicity island 1 (SPI-1) to inject effector proteins that mediate bacterial uptake. Only a subset of cells expresses flagella or the injectisome.
HilD is the master regulator of SPI-1. We showed that HilD directly activates transcription of flhDC. Expression of the injectisome and of flagella is therefore coupled at the level of the master regulators.
Together with the Klotzsch and Strowig groups, we found that induction of HilD reduced the motility of Salmonella, although HilD activates flhDC. The loss of motility required SPI-1 and depended on the proton motive force and on adhesins.
Expression of flagella and of SPI-1 is heterogeneous. We use dual fluorescent reporter strains in mother-machine devices to follow both programmes in single cells. We compare the wild type and regulatory mutants under different environmental conditions.
Contact: Hannah Raasch, E-mail
It is unknown how vT3SS substrates are selected from the cytoplasmic protein pool. We test the hypothesis that substrates are transcribed and translated close to the export apparatus. We combine genetic engineering with epifluorescence, TIRF, iSIM and STED microscopy and transcript localisation assays.
Contact: Hannah Grabietz, E-mail
