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Bernat Corominas-Murtra

Bernat Corominas-Murtra contributes to research discovery and scholarly infrastructure.

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Published work

3 published item(s)

preprint2026arXiv

A hyperbolic cell cycle law for early embryonic developmental timing

Across metazoans, early embryos exhibit a strikingly conserved slowing down of their cell duplication speed, despite widely varying developmental paces and underlying molecular mechanisms. Here we show that this common behavior arises because early development unfolds along a biochemical rather than a chronological timescale, resulting from the coupling of finite maternal resource consumption to the Michaelis-Menten-like kinetics governing the rates of the biochemical reactions involved in cell duplication. This leads to a hyperbolic growth of the Cell Cycle Length (CCL), approaching a mathematical singularity, which would correspond to developmental arrest. Data from a wide range of organisms -- cnidarians, nematodes, arthropods, molluscs, echinoderms, tunicates, amphibians, and fish -- collapse on a single curve, quantitatively capturing not only a universal CCL dynamical behaviour, but also key hallmarks of early metazoan development, including cell-number temporal evolution, the dependency of CCL on cell size, and, remarkably, gastrulation timing at the predicted singularity. Crucially, experimental modulation of resource availability and consumption rates validate the model and further demonstrate that a source of heterochrony in early development is an altered biochemical timescale of resource depletion. Overall, this work reveals resource consumption rates as a fundamental mechanism driving developmental timing in early embryogenesis across species.

preprint2022arXiv

The typical set and entropy in stochastic systems with arbitrary phase space growth

The existence of the {\em typical set} is key for data compression strategies and for the emergence of robust statistical observables in macroscopic physical systems. Standard approaches derive its existence from a restricted set of dynamical constraints. However, given the enormous consequences for the understanding of the system's dynamics, and its role underlying the presence of stable, almost deterministic statistical patterns, a question arises whether typical sets exist in much more general scenarios. We demonstrate here that the typical set can be defined and characterized from general forms of entropy for a much wider class of stochastic processes than it was previously thought. This includes processes showing arbitrary path dependence, long range correlations or dynamic sampling spaces; suggesting that typicality is a generic property of stochastic processes, regardless of their complexity. Our results impact directly in the understanding of the stability of complex systems, open the door to new data compression strategies and points to the existence of statistical mechanics-like approaches to systems arbitrarily away from equilibrium with dynamic phase spaces. We argue that the potential emergence of robust properties in complex stochastic systems provided by the existence of typical sets has special relevance to biological systems.

preprint2020arXiv

Stem cell lineage survival as a noisy competition for niche access

Understanding to what extent stem cell potential is a cell-intrinsic property, or an emergent behavior coming from global tissue dynamics and geometry, is a key outstanding question of systems and stem cell biology. Here, we propose a theory of stem cell dynamics as a stochastic competition for access to a spatially-localized niche, giving rise to a stochastic conveyor-belt model. Cell divisions produce a steady cellular stream which advects cells away from the niche, while random rearrangements enable cells away from the niche to be favourably repositioned. Importantly, even when assuming that all cells in a tissue are molecularly equivalent, we predict a common ("universal") functional dependence of the long-term clonal survival probability on distance from the niche, as well as the emergence of a well-defined number of functional stem cells, dependent only on the rate of random movements vs. mitosis-driven advection. We test the predictions of this theory on datasets on pubertal mammary gland tips, embryonic kidney tips as well homeostatic intestinal crypt. Importantly, we find good agreement for the predicted functional dependency of the competition as a function of position, and thus functional stem cell number in each organ. This argues for a key role of positional fluctuations in dictating stem cell number and dynamics, and we discuss the applicability of this theory to other settings.