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Molecular transport in living systems regulates numerous processes underlyingbiological function. Although many cellular components exhibit anomalousdiffusion, only recently has the subdiffusive motion been associated withnonergodic behavior. These findings have stimulated new questions for theirimplications in statistical mechanics and cell biology. Is nonergodicity acommon strategy shared by living systems? Which physical mechanisms generateit? What are its implications for biological function? Here, we use singleparticle tracking to demonstrate that the motion of DC-SIGN, a receptor withunique pathogen recognition capabilities, reveals nonergodic subdiffusion onliving cell membranes. In contrast to previous studies, this behavior isincompatible with transient immobilization and therefore it can not beinterpreted according to continuous time random walk theory. We show that thereceptor undergoes changes of diffusivity, consistent with the current view ofthe cell membrane as a highly dynamic and diverse environment. Simulationsbased on a model of ordinary random walk in complex media quantitativelyreproduce all our observations, pointing toward diffusion heterogeneity as thecause of DC-SIGN behavior. By studying different receptor mutants, we furthercorrelate receptor motion to its molecular structure, thus establishing astrong link between nonergodicity and biological function. These resultsunderscore the role of disorder in cell membranes and its connection withfunction regulation. Due to its generality, our approach offers a framework tointerpret anomalous transport in other complex media where dynamicheterogeneity might play a major role, such as those found, e.g., in softcondensed matter, geology and ecology.

Weak ergodicity breaking of receptor motion in living cells stemming from random diffusivity