ArticlePLoS computational biology2026
An agent-based model of Trypanosoma brucei social motility to explore determinants of colony pattern formation.
Article in PLoS computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
In vitro colonies of the unicellular parasite Trypanosoma brucei expand radially and establish fingering instabilities, a collective behavior known as social motility. The underlying mechanisms are thought to involve single-cell motility, chemical communication among cells, and mechanical interactions with the liquid boundary, but their relative contributions remain unclear. We aimed to determine which of the mechanisms are necessary to quantitatively reproduce the morphological characteristics of social motility. We developed a two-dimensional agent-based model that simulates colonies of 105-106 cells at single-cell resolution-two to four orders of magnitude larger than previous models. Cells are represented as point particles executing directional random walks with auto-chemotactic alignment and exponential colony growth. The colony boundary is modelled using a grid-based approach in which interactions with agents can locally weaken and expand it. The model was quantitatively evaluated by applying our previously established morphology metrics. We show quantitative agreement of the simulation results and experimental data in terms of colony morphology. Parameter exploration revealed that finger formation arises within a narrow range of trypanosome motility parameters that balance stochasticity and alignment, while boundary conditions modulate the speed of colony expansion. The diffusion coefficient of the chemotactic signal is the key determinant of pattern formation. Realistic behavior occurs at 2×10-11 - 10-10 m2/s which corresponds to molecules of 12.1-1690 kDa. These results demonstrate that complex colony morphologies can emerge from minimal cell-level rules, suggesting testable hypotheses for the molecular drivers of trypanosome social motility. Furthermore, our approach provides a framework for dissecting the interplay between motility, signaling, and mechanical confinement in other microbial systems exhibiting collective behavior.
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