Abstract
Spatially controlled polymerization of actin is at the origin of cell motility and is responsible for the formation of cellular protrusions like lamellipodia. The pathogens Listeria monocytogenes and Shigella flexneri, which undergo actin-based propulsion, are acknowledged models of the leading edge of lamellipodia. Actin-based motility of the bacteria or of functionalized microspheres can be reconstituted in vitro from only five pure proteins. Movement results from the regulated site-directed treadmilling of actin filaments, consistent with observations of actin dynamics in living motile cells and with the biochemical properties of the components of the synthetic motility medium.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Actin Depolymerizing Factors
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Actin-Related Protein 2
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Actin-Related Protein 3
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Actins / metabolism
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Actins / physiology*
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Adenosine Triphosphate / metabolism
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Animals
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Bacterial Proteins / metabolism
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Biopolymers
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Cell Movement*
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Cytoskeletal Proteins*
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Destrin
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Listeria monocytogenes / physiology*
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Microfilament Proteins / metabolism
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Models, Biological
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Movement
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Proteins / metabolism
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Pseudopodia / physiology
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Signal Transduction
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Wiskott-Aldrich Syndrome Protein
Substances
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Actin Depolymerizing Factors
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Actin-Related Protein 2
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Actin-Related Protein 3
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Actins
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Bacterial Proteins
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Biopolymers
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Cytoskeletal Proteins
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Destrin
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Microfilament Proteins
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Proteins
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Wiskott-Aldrich Syndrome Protein
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Adenosine Triphosphate