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Nonlinear biomolecular interactions on membranes drive membrane remodeling crucial for biological processes including chemotaxis, cytokinesis, and endocytosis. The complexity of biomolecular interactions, their redundancy, and the importance of spatiotemporal context in membrane organization impede understanding of the physical principles governing membrane mechanics. Developing a minimal in vitro system that mimics molecular signaling and membrane remodeling while maintaining physiological fidelity poses a major challenge. Inspired by chemotaxis, we reconstructed chemically regulated actin polymerization inside vesicles, guiding membrane self-organization. An external, undirected chemical input induced directed actin polymerization and membrane deformation uncorrelated with upstream biochemical cues, suggesting symmetry breaking. A biophysical model incorporating actin dynamics and membrane mechanics proposes that uneven actin distributions cause nonlinear membrane deformations, consistent with experimental findings. This protocellular system illuminates the interplay between actin dynamics and membrane shape during symmetry breaking, offering insights into chemotaxis and other cell biological processes. 

Mechanical rupture, or lysis, of the cytoplasmic membrane is a common cell death pathway in bacteria occurring in response to β-lactam antibiotics. A better understanding of the cellular design principles governing the susceptibility and response of individual cells to lysis could indicate methods of potentiating β-lactam antibiotics and clarify relevant aspects of cellular physiology. Here, we take a single-cell approach to bacterial cell lysis to examine three cellular features—turgor pressure, mechanosensitive channels, and cell shape changes—that are expected to modulate lysis. We develop a mechanical model of bacterial cell lysis and experimentally analyze the dynamics of lysis in hundreds of single Escherichia coli cells. We find that turgor pressure is the only factor, of these three cellular features, which robustly modulates lysis. We show that mechanosensitive channels do not modulate lysis due to insufficiently fast solute outflow, and that cell shape changes result in more severe cellular lesions but do not influence the dynamics of lysis. These results inform a single-cell view of bacterial cell lysis and underscore approaches of combatting antibiotic tolerance to β-lactams aimed at targeting cellular turgor. 

We study the low rank regression problem y = Mx + ε, where x and y are d1 and d2 dimensional vectors respectively. We consider the extreme high-dimensional setting where the number of observations n is less than d1 + d2. Existing algorithms are designed for settings where n is typically as large as rank(M)(d1+d2). This work provides an efficient algorithm which only involves two SVD, and establishes statistical guarantees on its performance. The algorithm decouples the problem by first estimating the precision matrix of the features, and then solving the matrix de-noising problem. To complement the upper bound, we introduce new techniques for establishing lower bounds on the performance of any algorithm for this problem. Our preliminary experiments confirm that our algorithm often out-performs existing baseline, and is always at least competitive. 

MreB is an actin homolog that is essential for coordinating the cell wall synthesis required for the rod shape of many bacteria. Previously we have shown that filaments of MreB bind to the curved membranes of bacteria and translocate in directions determined by principal membrane curvatures to create and reinforce the rod shape (Hussain et al., 2018). Here, in order to understand how MreB filament dynamics affects their cellular distribution, we model how MreB filaments bind and translocate on membranes with different geometries. We find that it is both energetically favorable and robust for filaments to bind and orient along directions of largest membrane curvature. Furthermore, significant localization to different membrane regions results from processive MreB motion in various geometries. These results demonstrate that the in vivo localization of MreB observed in many different experiments, including those examining negative Gaussian curvature, can arise from translocation dynamics alone.