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Register a new userSojourn-time distribution of virus capsid in interchromatin corrals of a cell nucleus
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Virus capsids in interchromatin corrals of a cell nucleus are experimentally known to exhibit anomalous diffusion as well as normal diffusion, leading to the Gaussian distribution of the diffusion-exponent fluctuations over the corrals. Here, the sojourn-time distribution of the virus capsid in local areas of the corral, i.e., probability distribution of the sojourn time characterizing diffusion in the local areas, is examined. Such an area is regarded as a virtual cubic block, the diffusion property in which is normal or anomalous. The distribution, in which the Gaussian fluctuation is incorporated, is shown to tend to slowly decay. Then, the block-size dependence of average sojourn time is discussed. A comment is also made on (non-)Markovianity of the process of moving through the blocks.
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In their work [Proc. Natl. Acad. Sci. USA 112 (2015) E5725], Bosse et al. experimentally showed that virus capsid exhibits not only normal diffusion but also anomalous diffusion in nucleus of a living cell. There, it was found that the distribution of fluctuations of the diffusion exponent characterizing them takes the Gaussian form, which is, quite remarkably, the same form for two different types of the virus. This suggests high robustness of such fluctuations. Here, the statistical property of local fluctuations of the diffusion exponent of the virus capsid in the nucleus is studied. A maximum-entropy-principle approach (originally proposed for a different virus in a different cell) is applied for obtaining the fluctuation distribution of the exponent. Largeness of the number of blocks identified with local areas of interchromatin corrals is also examined based on the experimental data. It is shown that the Gaussian distribution of the local fluctuations can be derived, in accordance with the above form. In addition, it is quantified how the fluctuation distribution on a long time scale is different from the Gaussian distribution.
Cell polarization underlies many cellular processes, such as differentiation, migration, and budding. Many living cells, such as budding yeast and fission yeast, use cytoskeletal structures to actively transport proteins to one location on the membrane and create a high density spot of membrane-bound proteins. Yet, the thermodynamic constraints on filament-based cell polarization remain unknown. We show by mathematical modeling that cell polarization requires detailed balance to be broken, and we quantify the free-energy cost of maintaining a polarized state of the cell. Our study reveals that detailed balance cannot only be broken via the active transport of proteins along filaments, but also via a chemical modification cycle, allowing detailed balance to be broken by the shuttling of proteins between the filament, membrane, and cytosol. Our model thus shows that cell polarization can be established via two distinct driving mechanisms, one based on active transport and one based on non-equilibrium binding. Furthermore, the model predicts that the driven binding process dissipates orders of magnitude less free-energy than the transport-based process to create the same membrane spot. Active transport along filaments may be sufficient to create a polarized distribution of membrane-bound proteins, but an additional chemical modification cycle of the proteins themselves is more efficient and less sensitive to the physical exclusion of proteins on the transporting filaments, providing insight in the design principles of the Pom1/Tea1/Tea4 system in fission yeast and the Cdc42 system in budding yeast.
Flagella of eukaryotic cells are transient long cylindrical protrusions. The proteins needed to form and maintain flagella are synthesized in the cell body and transported to the distal tips. What `rulers or `timers a specific type of cells use to strike a balance between the outward and inward transport of materials so as to maintain a particular length of its flagella in the steady state is one of the open questions in cellular self-organization. Even more curious is how the two flagella of biflagellates, like Chlamydomonas Reinhardtii, communicate through their base to coordinate their lengths. In this paper we develop a stochastic model for flagellar length control based on a time-of-flight (ToF) mechanism. This ToF mechanism decides whether or not structural proteins are to be loaded onto an intraflagellar transport (IFT) train just before it begins its motorized journey from the base to the tip of the flagellum. Because of the ongoing turnover, the structural proteins released from the flagellar tip are transported back to the cell body also by IFT trains. We represent the traffic of IFT trains as a totally asymmetric simple exclusion process (TASEP). The ToF mechanism for each flagellum, together with the TASEP-based description of the IFT trains, combined with a scenario of sharing of a common pool of flagellar structural proteins in biflagellates, can account for all key features of experimentally known phenomena. These include ciliogenesis, resorption, deflagellation as well as regeneration after selective amputation of one of the two flagella. We also show that the experimental observations of Ishikawa and Marshall are consistent with the ToF mechanism of length control if the effects of the mutual exclusion of the IFT trains captured by the TASEP are taken into account. Moreover, we make new predictions on the flagellar length fluctuations and the role of the common pool.
The infection pathway of virus in cytoplasm of a living cell is studied from the viewpoint of diffusion theory. The cytoplasm plays a role of a medium for stochastic motion of the virus contained in the endosome as well as the free virus. It is experimentally known that the exponent of anomalous diffusion fluctuates in localized areas of the cytoplasm. Here, generalizing fractional kinetic theory, such fluctuations are described in terms of the exponent locally distributed over the cytoplasm, and a theoretical proposition is presented for its statistical form. The proposed fluctuations may be examined in an experiment of heterogeneous diffusion in the infection pathway.
Living systems need to be highly responsive, and also to keep fluctuations low. These goals are incompatible in equilibrium systems due to the Fluctuation Dissipation Theorem (FDT). Here, we show that biological sensory systems, driven far from equilibrium by free energy consumption, can reduce their intrinsic fluctuations while maintaining high responsiveness. By developing a continuum theory of the E. coli chemotaxis pathway, we demonstrate that adaptation can be understood as a non-equilibrium phase transition controlled by free energy dissipation, and it is characterized by a breaking of the FDT. We show that the maximum response at short time is enhanced by free energy dissipation. At the same time, the low frequency fluctuations and the adaptation error decrease with the free energy dissipation algebraically and exponentially, respectively.
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