Biophysical modeling reveals hydrodynamic stress drives lipid uptake in prebiotic vesicles, suggesting a physical mechanism for early protocell growth.
In a previous work, we established that the mechanical agitation of the early Earth acts as a dissipative engine driving fatty acid vesicles through Critical Slowing Down (CSD) toward evolutionary stabilization via Szostak’s cannibalism. However, the precise molecular mechanism bridging macroscopic fluid shear stress and microscopic chemical assimilation remained a significant conceptual gap. This refinement paper provides the missing thermodynamic link by modeling the mechanochemical transduction at the colloidal interface. We demonstrate that hydrodynamic deformation alters the surface area-to-volume ratio of fluctuating vesicles, forcing hydrophobic tails into contact with water and spiking the local surface tension (γ). To alleviate this tension, single-chain amphiphile bilayers form transient toroidal nanopoores characterized by extreme local curvature. This structural disruption establishes a steep chemical potential gradient (\(μdeformed μmicelle\)), transforming the mechanically stressed vesicle into a thermodynamic sink that actively suctions surrounding lipid mass. This paper mathematically and conceptually bridges the gap between mechanical force and chemical affinity, formalizing the exact mechanism of prebiotic self-organization far from equilibrium.
No takes yet. Share an insight, caveat, or question.
Peter Mikuláš (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: