ArticlePLoS computational biology2009
An experimental and computational study of the effect of ActA polarity on the speed of Listeria monocytogenes actin-based motility.
Article in PLoS computational biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Motile and non-motile Listeria species adopt distinct ecological and evolutionary strategies to achieve broad geographic ranges across soil ecosystems.The ISME journal · 2026Article
- MEDYAN: Mechanochemical Simulations of Contraction and Polarity Alignment in Actomyosin Networks.PLoS computational biology · 2016Article
- Mesoscopic model of actin-based propulsion.PLoS computational biology · 2012Article
- Apparent diffusive motion of centrin foci in living cells: implications for diffusion-based motion in centriole duplication.Physical biology · 2011Article
- The roots of bioinformatics in theoretical biology.PLoS computational biology · 2011Article
- A microscopic formulation for the actin-driven motion of listeria in curved paths.Biophysical journal · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.