Active Instability and Nonlinear Dynamics of Cell-Cell Junctions.

Active cell-junction remodeling is important for tissue morphogenesis, yet its underlying physics is not understood. We study a mechanical model that describes junctions as dynamic active force dipoles. Their instability can trigger cell intercalations by a critical collapse.

Elasticity, Stability, and Quasioscillations of Cell-Cell Junctions in Solid Confluent Epithelia.

Macroscopic properties and shapes of biological tissues depend on the remodeling of cell-cell junctions at the microscopic scale. We propose a theoretical framework that couples a vertex model of solid confluent tissues with the dynamics describing generation of local force dipoles in the junctional actomyosin. Depending on the myosin turnover rate, junctions either preserve stable length or collapse to initiate cell rearrangements.

Desynchronization and pattern formation in a noisy feed-forward oscillator network.

We consider a one-dimensional directional array of diffusively coupled oscillators. They are perturbed by the injection of small additive noise, typically orders of magnitude smaller than the oscillation amplitude, and the system is studied in a region of the parameters that would yield deterministic synchronization. Non-normal directed couplings seed a coherent amplification of the perturbation: this latter manifests as a modulation, transversal to the limit cycle, which gains in potency node after node.

Noise-driven neuromorphic tuned amplifier.

We study a simple stochastic model of neuronal excitatory and inhibitory interactions. The model is defined on a directed lattice and internodes couplings are modulated by a nonlinear function that mimics the process of synaptic activation. We prove that such a system behaves as a fully tunable amplifier: the endogenous component of noise, stemming from finite size effects, seeds a coherent (exponential) amplification across the chain generating giant oscillations with tunable frequencies, a process that the brain could exploit to enhance, and eventually encode, different signals.

Intertangled stochastic motifs in networks of excitatory-inhibitory units.

A stochastic model of excitatory and inhibitory interactions which bears universality traits is introduced and studied. The endogenous component of noise, stemming from finite size corrections, drives robust internode correlations that persist at large distances. Antiphase synchrony at small frequencies is resolved on adjacent nodes and found to promote the spontaneous generation of long-ranged stochastic patterns that invade the network as a whole.