Abstract

Cell size is a key characteristic that significantly affects many aspects of cellular physiology. There are specific control mechanisms during cell cycle to maintain the cell size within a range from one generation to another. Such control mechanisms introduce substantial variability to important properties of the cell cycle such as inter-division time. To quantitatively study the effect of such variability in progression through cell cycle, detailed stochastic models are required. In this paper, a new hybrid stochastic model is proposed to study the effect of molecular noise and size control mechanism on the variabilities in cell cycle of the budding yeast Saccharomyces cerevisiae. The proposed model provides an accurate, yet computationally efficient approach for simulation of an intricate system by integrating the deterministic and stochastic simulation schemes.

Highlights

  • Cell size is a key characteristic that significantly affects many aspects of cellular physiology

  • We have shown that placing the dynamics of mRNAs into stochastic simulation algorithm (SSA) regime and solving ordinary differential equations (ODEs) for protein regulatory network leads to sufficiently accurate results, and significantly reduces the computational cost

  • We show that gene expression noise introduces significant variability to cell cycle

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Summary

Results

A new hybrid stochastic model is proposed to study the effect of molecular noise and size control mechanism on the variabilities in cell cycle of the budding yeast Saccharomyces cerevisiae. The proposed model provides an accurate, yet computationally efficient approach for simulation of an intricate system by integrating the deterministic and stochastic simulation schemes. The developed hybrid stochastic model can successfully capture several key features of the cell cycle observed in experimental data. The proposed model: 1) confirms that the majority of noise in size control stems from low copy numbers of transcripts in the G1 phase, 2) identifies the size and time regulation modules in the size control mechanism, and 3) conforms with phenotypes of early G1 mutants in exquisite detail

Conclusions
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