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Updated: Mar 13, 2026
11:10
High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
Published on: August 11, 2014
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TBK1 directs WIPI2 against Salmonella
Keith B Boyle1, Teresa L M Thurston2, Felix Randow1,3
1a MRC Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Francis Crick Avenue , Cambridge , UK.
Autophagy
|November 4, 2016
Summary
The kinase TBK1 is crucial for macroautophagy (autophagy) to capture invading Salmonella bacteria. TBK1 stabilizes WIPI2 on Salmonella, essential for early antibacterial autophagy steps and host defense.
Area of Science:
- Cellular microbiology
- Immunology
- Molecular biology
Background:
- Mammalian cells defend against Salmonella invasion via macroautophagy (autophagy).
- The kinase TBK1 regulates this crucial antibacterial process.
- Understanding TBK1's role in early autophagy is vital for host defense mechanisms.
Purpose of the Study:
- To investigate the novel function of TBK1 in controlling early antibacterial autophagy.
- To identify how TBK1 is recruited to Salmonella during invasion.
- To explore the evolutionary advantage of TBK1 recruitment redundancy.
Main Methods:
- Studied the interaction between TBK1, Salmonella, and WIPI2 in mammalian cells.
- Investigated the role of various 'eat-me' signals in recruiting TBK1.
- Analyzed the stabilization of WIPI2 on bacteria by TBK1 activity.
Main Results:
- TBK1 recruitment to Salmonella stabilizes the autophagy regulator WIPI2.
- This stabilization is essential for the early stages of antibacterial autophagy.
- TBK1 recruitment is redundant, triggered by multiple Salmonella-associated signals like glycans and ubiquitin chains.
Conclusions:
- TBK1 plays a novel, essential role in stabilizing WIPI2 for early antibacterial autophagy.
- Redundant recruitment mechanisms for TBK1 suggest an evolutionary advantage for host defense.
- This highlights a key host-pathogen interaction in cellular immunity.
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