Decoupling the Coupling: Surface Attachment in Actin-Based Motility

Tsuchida, Mark A.; Theriot, Julie A.

doi:10.1021/cb700071d

Cited by 3 publications

(3 citation statements)

References 23 publications

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“…In particular, comet tail organization and the trajectories of the virus were best explained by assuming continuous attachment of actin filament to the virus surface, supporting the hypothesis that tethering, possibly by VASP (Figure 1B) [28], which is present in the baculovirus tail, and pulling forces between the tail and the pathogen [17],[29] are needed to stabilize viral movement. A critical parameter influencing the modeling outcome was Brownian motion (see Text S1).…”

Section: Discussionsupporting

confidence: 59%

Electron Tomography and Simulation of Baculovirus Actin Comet Tails Support a Tethered Filament Model of Pathogen Propulsion

et al. 2014

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Section: Discussionsupporting

confidence: 59%

Electron Tomography and Simulation of Baculovirus Actin Comet Tails Support a Tethered Filament Model of Pathogen Propulsion

et al. 2014

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“…9,10,45 For Listeria, the surface protein ActA serves this function, and ActA's ability to support motility is greatly enhanced when it recruits the hostcell NPF, Vasodilator-stimulated Phosphoprotein (VASP), a member of the Ena/VASP and WASP (Wiskott Aldrich Syndrome Protein) family of NPF proteins. 8,9 Similarly, the microbial surface protein RickA 17 from Rickettsia and BimA 43 are bacterial analogues to Neuronal-WASP (N-WASP), whereas the Shigella surface protein IcsA captures the N-WASP from the host cell cytoplasm.…”

Section: Introductionmentioning

confidence: 99%

A Multi-Scale Mechanistic Model for Actin-Propelled Bacteria

Dickinson

2008

Cel. Mol. Bioeng.

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Some invasive bacterial pathogens propel themselves intracellularly by hijacking the host cell's actin assembly machinery to polymerize actin filaments into a dense ''comet tail'' network of filamentous actin. The bacterium is propelled forward as new actin monomers incorporate into filament ends positioned at the bacterial surface. How the bacterium remains firmly attached to the elongating end of the actin tail during propulsion remains a central question in actin-based motility. Here, a mechanistic model, based on the filament end-tracking motor (''actoclampin'') hypothesis, is proposed to explain some emergent features of actin-based propulsion, including the alignment of filaments with the direction of motion, rotation about the axis of motion, and helical trajectories. Simulation of the model shows that these features should arise naturally from diffusion-limited elongation of an ensemble of filaments that are strongly anchored at their elongating ends to the bacterial surface by end-tracking proteins. These results suggest that a persistent torsion and curvature of the actin comet tail does not require a filament torque (created by insertional elongation of helical filaments), although a small right-handed filament torque is sufficient to ensure symmetry breaking toward a right-handed torsion.

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“…All filaments are also able to retard the bacterium due to their interactions with the ActA protein, either directly or possibly via Arp2,3 or Ena/VASP, which create transient forces tethering the tail to the bacterium reviewed in [3],[19].…”

Section: Introductionmentioning

confidence: 99%

An Experimental and Computational Study of the Effect of ActA Polarity on the Speed of Listeria monocytogenes Actin-based Motility

2009

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Listeria monocytogenes is a pathogenic bacterium that moves within infected cells and spreads directly between cells by harnessing the cell's dendritic actin machinery. This motility is dependent on expression of a single bacterial surface protein, ActA, a constitutively active Arp2,3 activator, and has been widely studied as a biochemical and biophysical model system for actin-based motility. Dendritic actin network dynamics are important for cell processes including eukaryotic cell motility, cytokinesis, and endocytosis. Here we experimentally altered the degree of ActA polarity on a population of bacteria and made use of an ActA-RFP fusion to determine the relationship between ActA distribution and speed of bacterial motion. We found a positive linear relationship for both ActA intensity and polarity with speed. We explored the underlying mechanisms of this dependence with two distinctly different quantitative models: a detailed agent-based model in which each actin filament and branched network is explicitly simulated, and a three-state continuum model that describes a simplified relationship between bacterial speed and barbed-end actin populations. In silico bacterial motility required a cooperative restraining mechanism to reconstitute our observed speed-polarity relationship, suggesting that kinetic friction between actin filaments and the bacterial surface, a restraining force previously neglected in motility models, is important in determining the effect of ActA polarity on bacterial motility. The continuum model was less restrictive, requiring only a filament number-dependent restraining mechanism to reproduce our experimental observations. However, seemingly rational assumptions in the continuum model, e.g. an average propulsive force per filament, were invalidated by further analysis with the agent-based model. We found that the average contribution to motility from side-interacting filaments was actually a function of the ActA distribution. This ActA-dependence would be difficult to intuit but emerges naturally from the nanoscale interactions in the agent-based representation.

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Decoupling the Coupling: Surface Attachment in Actin-Based Motility

Cited by 3 publications

References 23 publications

Electron Tomography and Simulation of Baculovirus Actin Comet Tails Support a Tethered Filament Model of Pathogen Propulsion

Electron Tomography and Simulation of Baculovirus Actin Comet Tails Support a Tethered Filament Model of Pathogen Propulsion

A Multi-Scale Mechanistic Model for Actin-Propelled Bacteria

An Experimental and Computational Study of the Effect of ActA Polarity on the Speed of Listeria monocytogenes Actin-based Motility

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