Gene regulatory networks (GRNs) are fundamental to cellular growth and tissue formation, orchestrating spatially and temporally regulated gene expression during development. These networks are inherently subject to intrinsic fluctuations arising from molecular noise, making the analysis of their stability essential for understanding robust pattern formation and developmental dynamics of the organism. In this study, we analyze the stability and dynamics of cyclic GRNs with negative feedback and diffusion, considering both deterministic and stochastic approaches. In the deterministic case, the system exhibits a bifurcation between stability and instability, leading to Hopf instability in the absence of diffusion and to Turing-Hopf instability when diffusion is included. It was observed that the discretization of the spatial domain introduces additional unstable modes, enabling a wider range of patterns. The stochastic framework based on the second-moment approach, which incorporates intrinsic fluctuations, reveals that for small system sizes, fluctuations can dominate the dynamics and induce stochastic Turing instability, even when the system is stable in the absence of diffusion. Notably, Turing instabilities can emerge even when all variables have the same diffusion rate. The developed framework provides a systematic method for analyzing the stability of high-dimensional stochastic systems with diffusion, thereby simplifying the prediction of Turing and Turing-Hopf instabilities. These findings contribute to a deeper understanding of the complex dynamics and pattern formation in GRNs, with potential implications for biological processes, such as cellular differentiation and development.

Gene regulatory networks govern cellular fate decisions through multistable dynamics. The genetic toggle switch is a canonical model of such behaviour; yet, the impact of cell division on its dynamics remains poorly understood. We derive analytical separatrices for a simplified Boolean toggle switch with and without division. We show that division can redirect trajectories with identical initial conditions to opposing stable states, and we define a region of disagreement where fate decisions are predicted incorrectly if division is neglected. Our results imply that division can fundamentally reshape fate boundaries in multistable regulatory networks.

Imperfect molecular detection in single-cell experiments introduces technical noise that obscures the true stochastic dynamics of gene regulatory networks. While binomial models of molecular capture provide a principled description of imperfect detection, they have so far been analyzed only for simple gene-expression models that do not explicitly account for regulation. Here, we extend binomial models of capture to general gene regulatory networks to understand how imperfect capture reshapes the observed time-dependent statistics of molecular counts. Our results reveal when capture effects correspond to a renormalization of a subset of the kinetic rates and when they cannot be absorbed into effective rates, providing a systematic basis for interpreting noisy single-cell measurements. In particular, we show that rate renormalization depends on the level of regulatory detail in the model. For implicit regulatory models based on promoter state transitions, it arises whenever gene product synthesis does not trigger a promoter state change, as in the absence of promoter-proximal pausing or when pausing is short-lived. For models with explicit transcription factor binding, the same condition holds, together with sufficiently high transcription factor abundance, which in practice requires only a few tens of molecules per cell. In these cases, technical noise reduces the apparent mean burst size of synthesized gene products and accelerates the apparent rates of transcription factor binding reactions. This acceleration becomes stronger as the number of protein species and/or molecules involved in promoter switching increases. These effects hold for gene regulatory networks of arbitrary connectivity and remain valid under time-dependent kinetic rates.

Graph symmetries identify structural regularities and reduce the computational complexity of network analysis. In weighted graphs, however, exact automorphisms are rare because real-valued weights seldom coincide. We introduce a general framework for detecting approximate symmetries by aggregating weights into discrete categories, generating a sequence of coarser graphs on which classical automorphism analysis applies. The approximation path is fully configurable, based on interaction magnitudes, and can be matched to the empirical weight distribution. Applied to 250 empirical food webs using logarithmic aggregation, the method reveals that automorphisms emerge even at low approximation levels and almost always form small orbits. Orbit sizes rarely exceed two or three vertices, reflecting the combinatorial fragility of larger symmetric sets. Even so, symmetric vertices occupy diverse structural positions in the network and high connectivity does not imply asymmetry. The observation of just local permutations confirms the conclusions of trophic species and niche analysis. A case study demonstrates that automorphisms can also recover latent ecological structure. The minimal aggregation level at which two vertices become substitutable provides a quantitative measure of role similarity. The framework offers a principled, automorphism-based approach for quantifying similarity and redundancy in weighted complex networks.