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Bacterial populations typically exhibit exponential growth under resource-rich conditions, yet individual cells often deviate from this pattern. Recent work has shown that the elongation rates of and increase throughout the cell cycle (super-exponential growth), while displays a midcycle minimum (convex growth), and grows linearly. Here, we develop a single-cell model linking gene expression, proteome allocation, and mass growth to explain these diverse growth trajectories. By calibrating model parameters with experimental data, we show that DNA-proportional mRNA transcription produces near-exponential growth, whereas deviations from this proportionality yield the observed non-exponential growth patterns. Analysis of gene expression perturbations reveals that ribosome expression primarily controls dry mass growth rate, whereas cell envelope protein expression more strongly affects cell elongation rate. We show that cell-cycle-dependent transcription dynamics give rise to convex, super-exponential, and linear modes of cell elongation observed experimentally, demonstrating how the timing of cell envelope and ribosomal protein expressions drive cell-cycle-specific behaviors. These findings provide a mechanistic basis for non-exponential single-cell growth and offer insights into how bacterial cells dynamically regulate elongation rates within each generation. 

Accurate regulation of centrosome size is essential for ensuring error-free cell division, and dysregulation of centrosome size has been linked to various pathologies, including developmental defects and cancer. While a universally accepted model for centrosome size regulation is lacking, prior theoretical and experimental works suggest a centrosome growth model involving autocatalytic assembly of the pericentriolar material. Here, we show that the autocatalytic assembly model fails to explain the attainment of equal centrosome sizes, which is crucial for error-free cell division. Incorporating latest experimental findings into the molecular mechanisms governing centrosome assembly, we introduce a new quantitative theory for centrosome growth involving catalytic assembly within a shared pool of enzymes. Our model successfully achieves robust size equality between maturing centrosome pairs, mirroring cooperative growth dynamics observed in experiments. To validate our theoretical predictions, we compare them with available experimental data and demonstrate the broad applicability of the catalytic growth model across different organisms, which exhibit distinct growth dynamics and size scaling characteristics. 

Efficient allocation of energy resources to key physiological functions allows living organisms to grow and thrive in diverse environments and adapt to a wide range of perturbations. To quantitatively understand how unicellular organisms utilize their energy resources in response to changes in growth environment, we introduce a theory of dynamic energy allocation that describes cellular growth dynamics by partitioning metabolizable energy into key physiological functions: growth, division, cell shape regulation, energy storage and loss through dissipation. By optimizing the energy flux for growth, we develop the equations governing the time evolution of cell morphology and growth rate in diverse environments. The resulting model accurately captures experimentally observed dependencies of bacterial cell size on growth rate, superlinear scaling of metabolic rate with cell size and predicts nutrient-dependent trade-offs between energy expended for growth, division and shape maintenance. By calibrating model parameters with experimental data for the model organismEscherichia coli, our model describes bacterial growth control in dynamic conditions, particularly during nutrient shifts and osmotic shocks. Integrating both the mechanical properties of the cell and underlying biochemical regulation, our model predicts the driving factors behind a wide range of observed morphological and growth phenomena with minimal added complexity. 

Nuclear condensates play many important roles in chromatin functions, but how cells regulate their nucleation and growth within the complex nuclear environment is not well understood. Here, we report how condensate properties and chromatin mechanics dictate condensate growth dynamics in the nucleus. We induced condensates with distinct properties using different proteins in human cell nuclei and monitored their growth. We revealed two key physical mechanisms that underlie droplet growth: diffusion-driven or ripening-dominated growth. To explain the experimental observations, we developed a quantitative theory that uncovers the mechanical role of chromatin and condensate material properties in regulating condensate growth in a heterogeneous environment. By fitting our theory to experimental data, we find that condensate surface tension is critical in determining whether condensates undergo elastic or Ostwald ripening. Our model also predicts that chromatin heterogeneity can influence condensate nucleation and growth, which we validated by experimentally perturbing the chromatin organization and controlling condensate nucleation. By combining quantitative experimentation with theoretical modeling, our work elucidates how condensate surface tension and chromatin heterogeneity govern nuclear condensate ripening, implying that cells can control both condensate properties and the chromatin organization to regulate condensate growth in the nucleus. 

Abstract The accumulation and transmission of mechanical stresses in the cell cortex and membrane determines the mechanics of cell shape and coordinates essential physical behaviors, from cell polarization to cell migration. However, the extent that the membrane and cytoskeleton each contribute to the transmission of mechanical stresses to coordinate diverse behaviors is unclear. Here, we reconstitute a minimal model of the actomyosin cortex within liposomes that adheres, spreads and ultimately ruptures on a surface. During spreading, accumulated adhesion-induced (passive) stresses within the membrane drive changes in the spatial assembly of actin. By contrast, during rupture, accumulated myosin-induced (active) stresses within the cortex determine the rate of pore opening. Thus, in the same system, devoid of biochemical regulation, the membrane and cortex can each play a passive or active role in the generation and transmission of mechanical stress, and their relative roles drive diverse biomimetic physical behaviors.