Modeling of epidemic spreading with white Gaussian noise.

Motivated by the need to include the different characteristics of individuals and the damping effect in predictions of epidemic spreading, we build a model with variant coefficients and white Gaussian noise based on the traditional SIR model. The analytic and simulation results predicted by the model are presented and discussed. The simulations show that using the variant coefficients results in a higher percentage of susceptible individuals and a lower percentage of removed individuals. When the noise is included in the model, the percentage of infected individuals has a wider peak and more fluctuations than that predicted using the traditional SIR model.

Network Motifs Capable of Decoding Transcription Factor Dynamics.

Transcription factors (TFs) can encode the information of upstream signal in terms of its temporal activation dynamics. However, it remains unclear how different types of TF dynamics are decoded by downstream signalling networks. In this work, we studied all three-node transcriptional networks for their ability to distinguish two types of TF dynamics: amplitude modulation (AM), where the TF is activated with a constant amplitude, and frequency modulation (FM), where the TF activity displays an oscillatory behavior. We found two sets of network topologies: one set can differentially respond to AM TF signal but not to FM; the other set to FM signal but not to AM. Interestingly, there is little overlap between the two sets. We identified the prevalent topological features in each set and gave a mechanistic explanation as to why they can differentially respond to only one type of TF signal. We also found that some network topologies have a weak (not robust) ability to differentially respond to both AM and FM input signals by using different values of parameters for AM and FM cases. Our results provide a novel network mechanism for decoding different TF dynamics.

A systematic study of the determinants of protein abundance memory in cell lineage.

Proteins are essential players of life activities. Intracellular protein levels directly affect cellular functions and cell fate. Upon cell division, the proteins in the mother cell are inherited by the daughters. However, what factors and by how much they affect this epigenetic inheritance of protein abundance remains unclear. Using both computational and experimental approaches, we systematically investigated this problem. We derived an analytical expression for the dependence of protein inheritance on various factors and showed that it agreed with numerical simulations of protein production and experimental results. Our work provides a framework for quantitative studies of protein inheritance and for the potential application of protein memory manipulation.