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Widely used closed product-form networks have emerged recently as a primary model of stochastic growth of sub-cellular structures, e.g., cellular filaments. In the baseline model, homogeneous monomers attach and detach stochastically to individual filaments from a common pool of monomers, resulting in seemingly explicit product-form solutions. However, due to the large-scale nature of such networks, computing the partition functions for these solutions is numerically infeasible. To this end, we develop a novel methodology, based on a probabilistic representation of product-form solutions and large-deviations concentration inequalities, that yields explicit expressions for the marginal distributions of filament lengths. The parameters of the derived distributions can be computed from equations involving large-deviations rate functions, often admitting closed-form algebraic expressions. From a methodological perspective, a fundamental feature of our approach is that it provides exact results for order-one probabilities, even though our analysis involves large-deviations rate functions, which characterize only vanishing probabilities on a logarithmic scale.

Cells contain elaborate and interconnected networks of protein polymers which make up the cytoskeleton. The cytoskeleton governs the internal positioning and movement of vesicles and organelles, and controls dynamic changes in cell polarity, shape and movement. Many of these processes require tight control of the size and shape of cytoskeletal structures, which is achieved despite rapid turnover of their molecular components. Here we review mechanisms by which cells control the size of filamentous cytoskeletal structures from the point of view of simple quantitative models that take into account stochastic dynamics of their assembly and disassembly. Significantly, these models make experimentally testable predictions that distinguish different mechanisms of length-control. While the primary focus of this review is on cytoskeletal structures, we believe that the broader principles and mechanisms discussed herein will apply to a range of other subcellular structures whose sizes are tightly controlled and are linked to their functions., Comment: 61 pages, 11 figures

Actin cables are linear cytoskeletal structures that serve as tracks for myosin-based intracellular transport of vesicles and organelles in both yeast and mammalian cells. In a yeast cell undergoing budding, cables are in constant dynamic turnover yet some cables grow from the bud neck toward the back of the mother cell until their length roughly equals the diameter of the mother cell. This raises the question: how is the length of these cables controlled? Here we describe a novel molecular mechanism for cable length control inspired by recent experimental observations in cells. This antenna mechanism involves three key proteins: formins, which polymerize actin, Smy1 proteins, which bind formins and inhibit actin polymerization, and myosin motors, which deliver Smy1 to formins, leading to a length-dependent actin polymerization rate. We compute the probability distribution of cable lengths as a function of several experimentally tuneable parameters such as the formin-binding affinity of Smy1 and the concentration of myosin motors delivering Smy1. These results provide testable predictions of the antenna mechanism of actin-cable length control.

We review the recent discoveries of exotic heavy baryons at the Fermi National Accelerator Laboratory., Comment: 4 pages, 1 figure

We review the recent discoveries of rare oscillation phenomena in certain heavy neutral meson systems., Comment: 6 pages, 2 figures