Soft Matter and Complex Systems Seminar
sala 1.40, ul. Pasteura 5
2026-10-09 (09:30) 
Tomasz Skóra (IFT UW)
CELLestial mechanics: From passive crowding to active self-propulsion
Biomolecules, big or small, can perform their function only when they reach specific locations in a cell or encounter their specific counterparts. Thus, the intracellular mobility, the “CELLestial mechanics”, underlies the functioning of biological systems. In this talk, I will present two different faces of intracellular motion: passive diffusion – in which the intracellular milieu acts merely as an obstruction, and catalytically-driven self-propulsion – in which chemical reactions in cells enhance the diffusive motion.
Diffusivity in crowded environments is hindered for multiple reasons, among others: volume exclusion and hydrodynamic interactions. I will discuss the results of NMR measurements and Brownian/Stokesian dynamics simulations exploring the effect of tracer size and crowder concentration on metabolite diffusion. We observed a linear decrease in diffusivity with crowder volume fraction characterized by a metabolite size-dependent slope. While hard sphere models predict a linear increase of this slope with metabolite size, NMR data deviates from that prediction, pointing to the limitations of the underlying assumptions concerning crowders’ shape and interactions. This motivates my ongoing work using all-atom simulations to move beyond arbitrarily constructed, oversimplified coarse-grained representations.
Moving beyond passive transport, I will discuss how chemical reactions enhance intracellular diffusivity, drawing on our study of malaria parasites. Malaria parasites infect red blood cells and digest host hemoglobin. The released free heme is highly cytotoxic, promoting the formation of reactive oxygen species. To mitigate this threat, the parasite sequesters free heme into hemozoin nanocrystals inside a specialized digestive compartment called the food vacuole. Through quantitative in-cell image analysis, single-particle tracking and Brownian dynamics simulations, we showed that the motion of crystals is inconsistent with a model of passive Brownian motion, pointing instead to a local driving mechanism within the vacuole. We identified hydrogen peroxide as a source of this diffusion enhancement.
Diffusivity in crowded environments is hindered for multiple reasons, among others: volume exclusion and hydrodynamic interactions. I will discuss the results of NMR measurements and Brownian/Stokesian dynamics simulations exploring the effect of tracer size and crowder concentration on metabolite diffusion. We observed a linear decrease in diffusivity with crowder volume fraction characterized by a metabolite size-dependent slope. While hard sphere models predict a linear increase of this slope with metabolite size, NMR data deviates from that prediction, pointing to the limitations of the underlying assumptions concerning crowders’ shape and interactions. This motivates my ongoing work using all-atom simulations to move beyond arbitrarily constructed, oversimplified coarse-grained representations.
Moving beyond passive transport, I will discuss how chemical reactions enhance intracellular diffusivity, drawing on our study of malaria parasites. Malaria parasites infect red blood cells and digest host hemoglobin. The released free heme is highly cytotoxic, promoting the formation of reactive oxygen species. To mitigate this threat, the parasite sequesters free heme into hemozoin nanocrystals inside a specialized digestive compartment called the food vacuole. Through quantitative in-cell image analysis, single-particle tracking and Brownian dynamics simulations, we showed that the motion of crystals is inconsistent with a model of passive Brownian motion, pointing instead to a local driving mechanism within the vacuole. We identified hydrogen peroxide as a source of this diffusion enhancement.