BiPSim: a flexible and generic stochastic simulator for polymerization processes

Abstract

Detailed whole-cell modeling requires an integration of heterogeneous cell processes having different modeling formalisms, for which whole-cell simulation could remain tractable. Here, we introduce BiPSim, an open-source stochastic simulator of template-based polymerization processes, such as replication, transcription and translation. BiPSim combines an efficient abstract representation of reactions and a constant-time implementation of the Gillespie’s Stochastic Simulation Algorithm (SSA) with respect to reactions, which makes it highly efficient to simulate large-scale polymerization processes stochastically. Moreover, multi-level descriptions of polymerization processes can be handled simultaneously, allowing the user to tune a trade-off between simulation speed and model granularity. We evaluated the performance of BiPSim by simulating genome-wide gene expression in bacteria for multiple levels of granularity. Finally, since no cell-type specific information is hard-coded in the simulator, models can easily be adapted to other organismal species. We expect that BiPSim should open new perspectives for the genome-wide simulation of stochastic phenomena in biology.

NURR1 expression regulates retinal pigment epithelial–mesenchymal transition and age-related macular degeneration phenotypes

“…We report that dry AMD patients exhibit a significant reduction of NURR1 expression in the RPE cell layer, supporting a possible link between NURR1 and AMD progression. The presence of NURR1 immunoreactivity in spheroids within drusen may indicate that NURR1 fragments originate from RPE cells, given a number of drusen components derive from RPE cells ( 34 – 36 ); however, it is also plausible that they may come from the circulation and monocytes ( 37 ). In the future it would be important to evaluate potential correlations between NURR1 expression in the RPE across the different clinical stages of AMD, as well as the circulatory profile of NURR1 as a function of age and disease.…”