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Cells may control fluctuations in protein levels by means of negative autoregulation, where transcription factors bind DNA sites to repress their own production. Theoretical studies have assumed a single binding site for the repressor, while in most species it is found that multiple binding sites are arranged in clusters. We study a stochastic description of negative autoregulation with multiple binding sites for the repressor. We find that increasing the number of binding sites induces regular bursting of gene products. By tuning the threshold for repression, we show that multiple binding sites can also suppress fluctuations. Our results highlight possible roles for the presence of multiple binding sites of negative autoregulators.
Due to the stochastic nature of biochemical processes, the copy number of any given type of molecule inside a living cell often exhibits large temporal fluctuations. Here, we develop analytic methods to investigate how the noise arising from a bursti
Information transmission in biological signaling circuits has often been described using the metaphor of a noise filter. Cellular systems need accurate, real-time data about their environmental conditions, but the biochemical reaction networks that p
Multiple interlinked positive feedback loops shape the stimulus responses of various biochemical systems, such as the cell cycle or intracellular calcium release. Recent studies with simplified models have identified two advantages of coupling fast a
We introduce a minimal model description for the dynamics of transcriptional regulatory networks. It is studied within a mean-field approximation, i.e., by deterministic odes representing the reaction kinetics, and by stochastic simulations employing
A modified quantum teleportation protocol broadens the scope of the classical forbidden-interval theorems for stochastic resonance. The fidelity measures performance of quantum communication. The sender encodes the two classical bits for quantum tele