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Malti🦠 Cell Motility: Actin Polymerization & Crawling
Interactive biophysics simulation of amoeboid cell crawling. Watch actin treadmilling at the leading edge push the membrane forward via the Brownian ratchet, while actomyosin and focal adhesions drive the trailing edge.
About the Cell Motility Simulator
This simulation models amoeboid cell crawling — the mode of locomotion used by neutrophils chasing bacteria, fibroblasts closing a wound and invasive cancer cells. Each of the 26 filaments at the leading edge is tracked individually: monomers add stochastically to its barbed (+) end at rate k₊ᵦ·[G-actin] and leave its pointed (−) end at rate k₋ₚ − k₊ₚ·[G-actin], the real two-rate-constant kinetics first measured by Pollard. Because the barbed end has a lower critical concentration than the pointed end, a narrow window of free G-actin concentration makes filaments grow at one end while shrinking at the other — treadmilling — even though the filament's own length barely changes.
The net barbed-end growth is what pushes the membrane: this is the Brownian ratchet of Peskin, Odell and Oster. A thermally fluctuating membrane briefly opens a ≥2.7 nm gap, a monomer wedges in, and the now-longer, rigid filament prevents the membrane from drifting back — polymerization energy is ratcheted into mechanical protrusion. At the rear, actomyosin contraction pulls the trailing edge forward while integrin-based focal adhesions cycle between gripping the substrate and releasing it, producing the stepwise, stick-slip advance visible in the migration-speed readout.
Frequently Asked Questions
What does this cell motility simulator show?
It shows a crawling cell's leading-edge actin network in cross-section: individual filaments polymerizing at their barbed ends and depolymerizing at their pointed ends, pushing the front membrane forward while myosin contracts the rear and focal adhesions anchor and release along the substrate.
What is treadmilling?
Treadmilling is when a filament adds subunits at one end (barbed, +) at roughly the same rate it loses them at the other (pointed, −), so individual actin monomers appear to travel through the filament even though its overall length stays fairly constant.
What is the Brownian ratchet mechanism?
Proposed by Peskin, Odell and Oster, it explains how a soft, fluctuating membrane can be pushed by a growing filament even though the filament cannot literally shove it. Thermal motion occasionally opens a gap wide enough for a monomer to add; once added, the stiffened filament blocks the membrane from moving back, ratcheting each addition into forward progress.
Why do the sliders only affect the barbed on-rate and pointed off-rate?
Those are the two parameters cells actually regulate biologically — profilin and formins accelerate barbed-end addition, while ADF/cofilin severs and speeds pointed-end loss. The other two rate constants (barbed off-rate k₋ᵦ ≈ 1.4 s⁻¹ and pointed on-rate k₊ₚ ≈ 1.3 µM⁻¹s⁻¹) are held at their measured literature values so the treadmilling window stays realistic.
What happens if I set G-actin above 0.6 µM?
Above the pointed-end critical concentration (Cc(−) ≈ 0.6 µM) both ends gain subunits net — the filament simply grows longer everywhere and true treadmilling stops. Below the barbed-end critical concentration (Cc(+) ≈ 0.12 µM) the filament shrinks from both ends instead, mimicking a catastrophic loss of protrusive force.
Why does raising myosin strength not always speed up migration?
Migration speed in the model is limited by whichever end is slower — if actin polymerization can't keep pace, extra myosin contraction just increases rear tension against still-gripping focal adhesions without moving the cell faster, exactly as in real cells where protrusion and contraction must be coordinated.
What is the G-actin monomer pool and why does it deplete?
It represents the local free-monomer reservoir available to the leading edge. When the barbed-end on-rate is pushed high while the pool's resupply is limited, consumption outpaces diffusion resupply and the pool drains, throttling further growth — the same monomer-limited regime seen when cells over-express formins without matching profilin-actin.
What real cells crawl this way?
Neutrophils chasing bacterial chemoattractants, fibroblasts closing a wound, growth cones navigating during neural development, and invasive cancer cells all rely on lamellipodial actin treadmilling coupled to actomyosin contraction and adhesion turnover.
Why are the monomers color-graded along each filament?
It represents ATP hydrolysis: freshly added subunits near the barbed end carry ATP, which is hydrolyzed to ADP-Pi and then ADP as the subunit ages toward the pointed end. ADP-actin dissociates roughly ten times faster than ATP-actin, which is part of why depolymerization is concentrated at the pointed end.
Is this a physically accurate simulation?
The rate constants (k₊ᵦ, k₋ᵦ, k₊ₚ, k₋ₚ) and critical concentrations are literature values for skeletal-muscle actin. Kinetics are time-compressed for visibility and the membrane, adhesion cycling and myosin coupling are simplified aggregate models rather than a full mechanochemical simulation, but every control genuinely drives the underlying rate equations.
Interactive biophysics simulation of amoeboid cell crawling — watch actin treadmilling at the leading edge push the membrane forward via the Brownian ratchet mechanism.
2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install