Abstract
Cell growth is well described at the population level, but precisely how nutrient and water uptake and cell wall expansion drive the growth of single cells is poorly understood. Supported by measurements of single-cell growth trajectories and cell wall elasticity, we present a single-cell growth model for yeast. The model links the thermodynamic quantities, such as turgor pressure, osmolarity, cell wall elasto-plasticity, and cell size, applying concepts from rheology and thin shell theory. It reproduces cell size dynamics during single-cell growth, budding, and hyper-osmotic or hypo-osmotic stress. We find that single-cell growth rate and final size are primarily governed by osmolyte uptake and consumption, while bud expansion requires additionally different cell wall extensibilities between mother and bud. Based on first principles the model provides a more accurate description of size dynamics than previous attempts and its analytical simplification allows for easy combination with models for other cell processes.
Highlights
Cells are exposed to hydrostatic pressure driven by the difference between inner and outer osmolarity
We present a single-cell growth model (SCGM), which focuses on the interplay of three thermodynamic quantities: cell volume, osmolarity, and turgor pressure, and which covers growth and budding of single yeast cells as well as the response to external osmotic variations
To demonstrate that the SCGM can be combined with models for cellular signaling and metabolism, we introduced the high osmolarity glycerol (HOG) signaling cascade model[27] as an exemplary pathway that plays a major role in yeast osmoregulation.[2]
Summary
Cells are exposed to hydrostatic pressure driven by the difference between inner and outer osmolarity. Thermodynamic descriptions of volume and pressure changes were integrated within the osmotic stress response system, i.e. the high osmolarity glycerol (HOG) signaling pathway, metabolism, and gene expression.[3] This integrative model permitted predictions regarding the effect of several geneknockouts on volume dynamics Another model integrated further published data with biophysical and mechanical properties of yeast to describe the loss in volume immediately after osmotic stress.[4] Both models explain volume regulation following a hyperosmotic shock, but are not designed to describe the small and steady volume variations during normal growth. To demonstrate that the SCGM can be combined with models for cellular signaling and metabolism, we introduced the HOG signaling cascade model[27] as an exemplary pathway that plays a major role in yeast osmoregulation.[2]
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