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Aneta Koseska

Publications and source records attributed to Aneta Koseska.

6 recordsLinked to original sources

Unifying Theories in High-Dimensional Biology: Approaches, Challenges and Opportunities

Across biological subdisciplines, the last decade has seen an explosion of high-dimensional datasets, including datasets for cells, species, immune systems, neurons and behaviour. At the ICTS workshop 'Unifying Theories in High-Dimensional Biophysics' we discussed whether this high dimensionality poses a challenge or opportunity for describing, understanding and predicting biological systems theoretically. We discussed methods, models and frameworks that can help with addressing empirical observations based on these high-dimensional datasets. We summarize the challenges and opportunities that emerged in discussions according to individual participants below.

physics.bio-ph

Oscillation Quenching Induced By Time-Varying Coupling Functions

The oscillatory dynamics of natural and man-made systems can be disrupted by their time-varying interactions, leading to oscillation quenching phenomena in which the oscillations are suppressed. We introduce a framework for analyzing, assessing, and controlling oscillation quenching using coupling functions. Specifically, by observing limit-cycle oscillators we investigate the bifurcations and dynamical transitions induced by time-varying diffusive and periodic coupling functions. We studied the transitions between oscillation quenching states induced by the time-varying form of the coupling function while the coupling strength is kept invariant. The time-varying periodic coupling function allowed us to identify novel, non-trivial inhomogeneous states that have not been reported previously. Furthermore, by using dynamical Bayesian inference we have also developed a Proportional Integral (PI) controller that maintains the oscillations and \red{prevents oscillation quenching from occurring}. In addition to the present implementation and its generalizations, the framework carries broader implications for identification and control of oscillation quenching in a wide range of systems subjected to time-varying interactions.

nlin.AO

Biological computations: limitations of attractor-based formalisms and the need for transients

Living systems, from single cells to higher vertebrates, receive a continuous stream of non-stationary inputs that they sense, e.g., via cell surface receptors or sensory organs. Integrating these time-varying, multi-sensory, and often noisy information with memory using complex molecular or neuronal networks, they generate a variety of responses beyond simple stimulus-response association, including avoidance behavior, life-long-learning or social interactions. In a broad sense, these processes can be understood as a type of biological computation. Taking as a basis generic features of biological computations, such as real-time responsiveness or robustness and flexibility of the computation, we highlight the limitations of the current attractor-based framework for understanding computations in biological systems. We argue that frameworks based on transient dynamics away from attractors are better suited for the description of computations performed by neuronal and signaling networks. In particular, we discuss how quasi-stable transient dynamics from ghost states that emerge at criticality have a promising potential for developing an integrated framework of computations, that can help us understand how living system actively process information and learn from their continuously changing environment.

q-bio.OT

Ghost cycles exhibit increased entrainment and richer dynamics in response to external forcing compared to slow-fast systems

Many natural, living and engineered systems display oscillations that are characterized by multiple timescales. Typically, such systems are described as slow-fast systems, where the slow dynamics result from a hyperbolic slow manifold that guides the movement of the system trajectories. Recently, we have provided an alternative description in which the slow dynamics result from a non-hyperbolic and Lyapunov-unstable attracting sets from connected dynamical ghosts that form a closed orbit (termed ghost cycles). Here we investigate the response properties of both type of systems to external forcing. Using the classical Van-der-Pol oscillator and two modified versions of this model that correspond to a 1-ghost and a 2-ghost cycle, respectively, we find that ghost cycles are characterized by significant increase especially in the 1:1 entrainment regions as demonstrated by the corresponding Arnold tongues and exhibit richer dynamics (bursting, chaos) in contrast to the classical slow-fast system. Phase plane analysis reveals that these features result from the continuous remodeling of the attractor landscape of the ghost cycles models characteristic for non-autonomous systems, whereas the attractor landscape of the corresponding slow-fast system remains qualitatively unaltered. We propose that systems containing ghost cycles display increased flexibility and responsiveness to continuous environmental changes.

nlin.AO

Ghost channels and ghost cycles guiding long transients in dynamical systems

Dynamical descriptions and modeling of natural systems have generally focused on fixed points, with saddles and saddle-based phase-space objects such as heteroclinic channels/cycles being central concepts behind the emergence of quasi-stable long transients. Reliable and robust transient dynamics observed for real, inherently noisy systems is, however, not met by saddle-based dynamics, as demonstrated here. Generalizing the notion of ghost states, we provide a complementary framework that does not rely on the precise knowledge or existence of (un)stable fixed points, but rather on slow directed flows organized by ghost sets in ghost channels and ghost cycles. Moreover, we show that appearance of these novel objects is an emergent property of a broad class of models, typically used for description of natural systems.

physics.bio-ph

Cooperative regulation of cellular identity in systems with intercellular communication defects

The cooperative dynamics of cellular populations emerging from the underlying interactions determines cellular functions, and thereby their identity in tissues. Global deviations from this dynamics on the other hand reflects pathological conditions. However, how these conditions are stabilized from dis-regulation on the level of the single entities is still unclear. Here we tackle this question using generic Hodgkin-Huxley type of models that describe physiological bursting dynamics of pancreatic beta-cells, and introduce channel dis-function to mimic pathological silent dynamics. The probability for pathological behavior in beta-cell populations is $\sim100\%$ when all cell have these defects, despite the negligible size of the silent state basin of attraction for single cells. In stark contrast, in a more realistic scenario for a heterogeneous population, stabilization of the pathological state depends on the size of the sub-population which acquired the defects. However, the probability to exhibit stable pathological dynamics in this case is less than $\sim10\%$. These results therefore suggest that the physiological bursting dynamics of a population of beta-cells is cooperatively regulated, even under intercellular communication defects induced by dis-functional channels of single-cells.

q-bio.CB