Cadherin expression is required for the spread of Shigella flexneri between epithelial cells

Sansonetti, Philippe J.; Mounier, Joëlle; Prévost, Marle Christine; Mège, René-Marc

doi:10.1016/0092-8674(94)90358-1

Cited by 163 publications

(90 citation statements)

References 37 publications

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“…Both myosin II and myosin light-chain kinase are required for formation of these protrusions into neighboring cells (37). Cadherins and connexin 26 are required for bacterial spread, suggesting that Shigella interacts with the proteins mediating cellto-cell contacts (41,50). Host cell proteins regulating actin polymerization are also required, including N-WASP and profilin (27).…”

Section: Resultsmentioning

confidence: 99%

Abl Kinases Regulate Actin Comet Tail Elongation via an N-WASP-Dependent Pathway

Burton¹,

Oliver

Pendergast³

2005

Molecular and Cellular Biology

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Microbial pathogens have evolved diverse strategies to modulate the host cell cytoskeleton to achieve a productive infection and have proven instrumental for unraveling the molecular machinery that regulates actin polymerization. Here we uncover a mechanism for Shigella flexneri-induced actin comet tail elongation that links Abl family kinases to N-WASP-dependent actin polymerization. We show that the Abl kinases are required for Shigella actin comet tail formation, maximal intracellular motility, and cell-to-cell spread. Abl phosphorylates N-WASP, a host cell protein required for actin comet tail formation, and mutation of the Abl phosphorylation sites on N-WASP impairs comet tail elongation. Furthermore, we show that defective comet tail formation in cells lacking Abl kinases is rescued by activated forms of N-WASP. These data demonstrate for the first time that the Abl kinases play a role in the intracellular motility and intercellular dissemination of Shigella and uncover a new role for Abl kinases in the regulation of pathogen motility.

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Section: Resultsmentioning

confidence: 99%

Abl Kinases Regulate Actin Comet Tail Elongation via an N-WASP-Dependent Pathway

Burton¹,

Oliver

Pendergast³

2005

Molecular and Cellular Biology

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“…It has been described that S. flexneri localizes to adherence junctions (22). Together with the observation that E-cadherin expression appears to be necessary for cell-to-cell spread (23), it is now tempting to investigate whether SfHtrA-mediated E-cadherin cleavage may be involved in S. flexneri intercellular spreading. In fact, HtrA is required for IcsA expression and S. flexneri uptake (24).…”

Section: Discussionmentioning

confidence: 99%

Distinct Roles of Secreted HtrA Proteases from Gram-negative Pathogens in Cleaving the Junctional Protein and Tumor Suppressor E-cadherin

Hoy

Geppert

Boehm

et al. 2012

Journal of Biological Chemistry

148

194

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“…Transmission electron micrographs have captured a few intermediate steps that show membrane-bound protrusions of S. flexneri invading neighbouring cells (Kadurugamuwa et al, 1991;Sansonetti et al, 1994;Schuch et al, 1999). No protein has yet been identified in S. flexneri that is necessary for mediating the intermediate step in cell-to-cell spread or protrusion uptake.…”

Section: Introductionmentioning

confidence: 99%

“…Within the host cell cytoplasm, the bacteria continue to grow and divide and move rapidly through the cell by nucleating actin filaments at one pole of the bacterium, leaving behind actin-rich`comet tails' in the cytoplasm (Ogawa et al, 1968;Bernardini et al, 1989;Pal et al, 1989). Shigella spread from an infected cell to uninfected neighbours through membrane-bound protrusions (Kadurugamuwa et al, 1991;Prevost et al, 1992;Sansonetti et al, 1994). Bacterial actin-based motility is necessary for intercellular spread in tissue culture monolayers and for virulence in infected animals .…”

Section: Introductionmentioning

confidence: 99%

Actin-based motility is sufficient for bacterial membrane protrusion formation and host cell uptake

Monack

Theriot

2001

Cellular Microbiology

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SummaryShigella flexneri replicates in the cytoplasm of host cells, where it nucleates host cell actin filaments at one pole of the bacterial cell to form a`comet tail' that propels the bacterium through the host's cytoplasm. To determine whether the ability to move by actinbased motility is sufficient for subsequent formation of membrane-bound protrusions and intercellular spread, we conferred the ability to nucleate actin on a heterologous bacterium, Escherichia coli. Previous work has shown that IcsA (VirG), the molecule that is necessary and sufficient for actin nucleation and actin-based motility, is distributed in a unipolar fashion on the surface of S. flexneri. Maintenance of the unipolar distribution of IcsA depends on both the S. flexneri outer membrane protease IcsP (SopA) and the structure of the lipopolysaccharide (LPS) in the outer membrane. We co-expressed IcsA and IcsP in two strains of E. coli that differed in their LPS structures. The E. coli were engineered to invade host cells by expression of invasin from Yersinia pseudotuberculosis and to escape the phagosome by incubation in purified listeriolysin O (LLO) from Listeria monocytogenes. All E. coli strains expressing IcsA replicated in host cell cytoplasm and moved by actin-based motility. Actin-based motility alone was sufficient for the formation of membrane protrusions and uptake by recipient host cells. The presence of IcsP and an elaborate LPS structure combined to enhance the ability of E. coli to form protrusions at the same frequency as S. flexneri, quantitatively reconstituting this step in pathogen intercellular spread in a heterologous organism. The frequency of membrane protrusion formation across all strains tested correlates with the efficiency of unidirectional actin-based movement, but not with bacterial speed.

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Cadherin expression is required for the spread of Shigella flexneri between epithelial cells

Cited by 163 publications

References 37 publications

Abl Kinases Regulate Actin Comet Tail Elongation via an N-WASP-Dependent Pathway

Abl Kinases Regulate Actin Comet Tail Elongation via an N-WASP-Dependent Pathway

Distinct Roles of Secreted HtrA Proteases from Gram-negative Pathogens in Cleaving the Junctional Protein and Tumor Suppressor E-cadherin

Actin-based motility is sufficient for bacterial membrane protrusion formation and host cell uptake

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