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Published on: September 5, 2019
A biological interpretation of transient anomalous subdiffusion. I. Qualitative model
1Department of Biochemistry and Molecular Medicine, University of California, Davis, California 95616, USA. mjsaxton@ucdavis.edu
Anomalous subdiffusion occurs in biological systems due to binding sites and barriers. A finite hierarchy of binding sites leads to anomalous diffusion at short times and normal diffusion at long times.
Area of Science:
- Biophysics
- Cellular Biology
- Physical Chemistry
Background:
- Anomalous subdiffusion is observed in biological environments like the plasma membrane, nucleus, and cytoplasm.
- Particle diffusion can be anomalous over time, influenced by binding sites and barriers.
Purpose of the Study:
- To investigate the impact of binding site hierarchies and thermal equilibrium on anomalous subdiffusion.
- To develop a physical model for anomalous subdiffusion that can be tested in biological systems.
Main Methods:
- Monte Carlo calculations were used to simulate diffusion in a hierarchy of binding sites.
- The anomalous diffusion exponent and the duration of anomalous diffusion were determined.
- The influence of thermal equilibrium on diffusion in the presence of binding sites and barriers was analyzed.
Main Results:
- Finite hierarchies of binding sites result in anomalous diffusion at short times and normal diffusion at long times.
- Even a single binding site can cause a brief period of anomalous subdiffusion.
- Anomalous subdiffusion due to barriers persists at thermal equilibrium, while binding-site-induced anomalous subdiffusion is reduced but not eliminated.
Conclusions:
- The presence and structure of binding sites significantly influence diffusion dynamics.
- Thermal equilibrium affects anomalous subdiffusion differently depending on whether it is caused by binding sites or barriers.
- The developed physical model provides a framework for understanding and experimentally testing anomalous subdiffusion in biological contexts using single-particle tracking.
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