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Updated: May 29, 2025

Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
Published on: September 19, 2013
Characterization of c-Src During Listeria monocytogenes Cell-to-Cell Spreading
Petra McLeod1, Aaron S Dhanda1, Julian A Guttman1
1Department of Biological Sciences, Centre for Cell Biology, Development, and Disease (C2D2), Simon Fraser University, 8888 University Dr W, Burnaby, BC, V5A 1S6, Canada.
Abstract:
Listeria monocytogenes replicates within host cells and spreads from cell to cell using actin-based motility. Cell-to-cell movement of L. monocytogenes is achieved by creating actin-rich membrane protrusions (listeriopods), which generate corresponding invaginations in adjacent cells through caveolin-mediated endocytosis. We show that c-Src, a multifunctional tyrosine kinase, is enriched at invaginations and is crucial for efficient cell-to-cell spreading of the bacteria as cells expressing c-Src mutants that were either constitutively active or those that impeded the function of c-Src resulted in significantly more (or less) cell-to-cell spreading. This work demonstrates the importance of c-Src in influencing L. monocytogenes' ability to spread intercellularly.
Insights
Listeria monocytogenes spreads between cells using actin motility. The tyrosine kinase c-Src is essential for this bacterial cell-to-cell spread, influencing bacterial invasion and movement.
Area of Science:
- Microbiology
- Cell Biology
- Biochemistry
Background:
- Listeria monocytogenes is an intracellular bacterium that spreads between host cells.
- Bacterial cell-to-cell spread relies on actin-based motility and the formation of membrane protrusions.
Purpose of the Study:
- To investigate the role of c-Src in the cell-to-cell spreading of Listeria monocytogenes.
- To elucidate the mechanism by which c-Src influences bacterial intercellular motility.
Main Methods:
- Analysis of c-Src localization during Listeria monocytogenes infection.
- Assessment of bacterial cell-to-cell spread in cells expressing wild-type and mutant c-Src.
- Utilizing caveolin-mediated endocytosis pathways.
Main Results:
- c-Src is enriched at membrane invaginations mediating bacterial entry into adjacent cells.
- Expression of constitutively active or non-functional c-Src mutants significantly altered Listeria monocytogenes cell-to-cell spreading.
- c-Src activity is crucial for efficient intercellular spread.
Conclusions:
- c-Src plays a critical role in Listeria monocytogenes intercellular spread.
- The tyrosine kinase c-Src is a key host factor influencing bacterial dissemination.
- Targeting c-Src could potentially inhibit the spread of L. monocytogenes.
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