The molecular mechanism of virulence effector protein translocation by Salmonella SipB. (360G-Wellcome-105390_Z_14_Z)
A critical step in pathogenesis of enteric bacteria such as Salmonella is hijacking the host cell. This event depends on the type three secretion system (T3SS) which enables the delivery of subversive virulence effectors into the host 3,11. A hydrophobic protein called SipB is part of the T3SS and forms the translocon element 3. While the mechanism of effector translocation across the host cell plasma membrane remains elusive, previous work in our lab revealed that SipB is essential for translocation and has liposome fusion activity 7. When fusion is inhibited with a truncated derivative of SipB (SipB428-593), Salmonella entry into host cells is prevented6. The aim of this project is to build upon this foundation to research the mechanism of effector delivery into host cells. We will use established in vitro liposome fusion assays – together with biochemical reconstitution and high-resolution structural studies – to reveal the mechanism of translocation. Following the successful work with SipB 428-593, we aspire to screen natural extracts and synthetic compound libraries in search of a T3SS inhibitor, which could have therapeutic value. Finally, we will also extend our work onto homologous T3S systems from other pathogens, such as Shigella, Yersinia and E. coli.
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Grant Details
Amount Awarded | 160792 |
Applicant Surname | Wolanska |
Approval Committee | PhD Studentships |
Award Date | 2014-07-14T00:00:00+00:00 |
Financial Year | 2013/14 |
Grant Programme: Title | PhD Studentship (Basic) |
Internal ID | 105390/Z/14/Z |
Lead Applicant | Ms Dominika Wolanska |
Partnership Value | 160792 |
Planned Dates: End Date | 2018-09-30T00:00:00+00:00 |
Planned Dates: Start Date | 2014-10-01T00:00:00+00:00 |
Recipient Org: Country | United Kingdom |
Region | East of England |
Sponsor(s) | Prof Paul Lehner |