Cells are known to utilize biochemical noise to probabilistically switch between distinct gene expression states. We demonstrate that such noise-driven switching is dominated by tails of probability distributions and is therefore exponentially sensit
ive to changes in physiological parameters such as transcription and translation rates. However, provided mRNA lifetimes are short, switching can still be accurately simulated using protein-only models of gene expression. Exponential sensitivity limits the robustness of noise-driven switching, suggesting cells may use other mechanisms in order to switch reliably.
Chemotaxis receptors in E. coli form clusters at the cell poles and also laterally along the cell body, and this clustering plays an important role in signal transduction. Recently, experiments using flourrescence imaging have shown that, during cell
growth, lateral clusters form at positions approximately periodically spaced along the cell body. In this paper, we demonstrate within a lattice model that such spatial organization could arise spontaneously from a stochastic nucleation mechanism. The same mechanism may explain the recent observation of periodic aggregates of misfolded proteins in E. coli.
