We build physical models of living systems and processes using tools from theoretical physics, applied mathematics, and systems biology. Our goal is to uncover the quantitative principles governing how cells and organisms self-organize, change shape, adapt, and build functional structures. Our work is highly cross-disciplinary, performed in close collaboration with experimentalists.
Individual cells are remarkably adept at sensing, responding to, and even anticipating changes in their environment. Understanding how this adaptive capacity emerges from molecular-level processes, without a nervous system or centralized controller, is one of the most fascinating open questions at the boundary of physics and biology.
We use bacteria as a model system to develop quantitative theories of single-cell physiology. Our work addresses two interconnected questions. First, how do cells regulate their growth, size, and shape? Bacteria maintain precise control over their geometry through nutrient-dependent allocation of cellular resources between growth and division machinery, and through physical constraints linking surface-to-volume scaling to morphology. Second, how do cells adapt to environmental stress? We have shown that bacteria deploy multi-timescale strategies to survive antibiotic challenge, coupling mechanical feedback and gene expression remodelling to navigate hostile conditions. Most recently, we have found that single bacterial cells can exhibit emergent learning-like behaviour, adjusting their physiological state across multiple timescales in ways that resemble adaptive memory.
A recurring theme in our work is that single-cell behaviour is shaped by physical constraints and tradeoffs, not just molecular circuits. Resource competition, mechanical feedback, and stochastic fluctuations are as important as regulatory networks in determining how a cell grows, divides, and survives.
Tissues are far more than collections of cells. Through local mechanical interactions and biochemical signaling, cells collectively generate forces, remodel their contacts, and coordinate shape changes across length scales that far exceed any individual cell. How these local rules give rise to tissue-scale form and function is a central question in developmental biology, and one that is deeply amenable to physical modeling.
Our work focuses on the feedback between mechanical forces and biochemical signaling as a core organizing principle of tissue behavior. We have shown that mechanosensitive junction remodeling allows epithelial tissues to robustly change shape during morphogenesis, that tension remodeling drives topological rearrangements in cell packings, and that excitable mechanical waves can propagate across tissues through force-dependent signaling. A recurring finding is that tissues operate near dynamical instabilities: small perturbations in mechanical feedback can switch collective behavior between ordered and disordered, proliferating and arrested, fluid and solid states.
We are particularly interested in the physics of tissue morphogenesis during embryonic development. Working closely with experimental collaborators, we have developed physical models for hindbrain neuropore closure in mouse embryos, revealing how tissue geometry and cell-generated forces combine to drive asymmetric, coordinated closure. More broadly, we study how cell competition, proliferation, and adhesion remodeling shape the mechanical state of growing tissues, and how epithelial monolayers learn and adapt their elastic properties through local tension remodeling.
Living cells contain a remarkable variety of subcellular structures, including organelles, biomolecular condensates, and cytoskeletal assemblies, each built to micron-scale specifications from a shared inventory of molecular components. How cells achieve this precision, and how they maintain it as conditions change, is a central open question in cell biology.
We develop theoretical models for the self-assembly, self-organization, and size control of intracellular structures. Our work spans three connected directions: (i) organelle size regulation through shared pools of subunits and feedback mechanisms that couple growth to component availability; (ii) biomolecular condensates and how their material properties interact with the cellular environment to control nucleation and ripening; and (iii) the actin cytoskeleton as an active adaptive material whose mechanical and architectural properties emerge from the collective dynamics of filaments, motors, and crosslinkers.
A unifying theme is that intracellular structures are not built to fixed blueprints. Instead, their size, composition, and dynamics emerge from physical principles: limiting pools, biochemical feedback, phase separation, and active stress generation, which we aim to formalise quantitatively.