Papers

During development, embryos store, transmit, and transform information to generate spatial patterns. Positional information (PI) quantifies how precisely cells form patterns at a given time, but cell motion has limited its application to static tissues. We introduce a framework for PI in dynamic tissues by decomposing mutual information between cells' positions and properties over time into information flows contributing to PI preservation, loss and generation. These reveal information-theoretic signatures of ubiquitous developmental processes, including instruction, sorting and mixing, directly from data. Applying this framework to whole-embryo cell trajectories in Drosophila, mouse and zebrafish gastrulation, we provide local and global information-theoretic quantification of cell mixing and derive bounds on PI preservation imposed by tissue dynamics. Analyzing tissue flows as dynamical systems, we further show that morphogenesis structures mixing, preferentially preserving specific patterns. Finally, we derive inequality conditions for tracing generated PI to candidate information sources and distinguishing among alternative pattern-formation mechanisms, from programmed extracellular cues to self-organizing intercellular interactions.

doi: 10.64898/2026.04.15.718553

Embryogenesis integrates morphogenesis - coordinated cell movements - with morphogen patterning and cell differentiation. While largely studied independently, morphogenesis and patterning often unfold simultaneously in early embryos. Yet how cell movements affect morphogen transport and cells' exposure over time remains unclear, as most pattern formation models assume static tissues. Here we develop a theoretical framework for morphogen patterning in dynamic tissues, recasting advection-reaction-diffusion equations in the cells' moving reference frames. This framework (i) elucidates how morphogenesis mediates morphogen transport and compartmentalization: cell-cell diffusive transport is enhanced at multicellular flow attractors, while repellers act as barriers, affecting cell fate induction and bifurcations. (ii) It formalizes cell-cell signaling ranges in dynamic tissues, deconfounding morphogenetic movements to identify which cells could communicate via morphogens. (iii) It provides two new nondimensional numbers to assess when and where morphogenesis affects morphogen transport. We demonstrate this framework by analyzing classical patterning models with common morphogenetic motifs as well as experimental tissue flows. Our work rationalizes dynamic tissue patterning in development, constraining candidate patterning mechanisms and parameters using accessible cell motion data.

doi: 10.1103/h74q-3dgj

Autocatalysis is thought to have played an important role in the earliest stages of the origin of life. An autocatalytic cycle (AC) is a set of reactions that results in stoichiometric increase in its constituent chemicals. When the reactions of multiple interacting ACs are active in a region of space, they can have interactions analogous to those between species in biological ecosystems. Prior studies of autocatalytic chemical ecosystems (ACEs) have suggested avenues for accumulating complexity, such as ecological succession, as well as obstacles such as competitive exclusion. We extend this ecological framework to investigate the effects of surface adsorption, desorption, and diffusion on ACE ecology. Simulating ACEs as particle-based stochastic reaction-diffusion systems in spatial environments-including open, two-dimensional reaction-diffusion systems and adsorptive mineral surfaces-we demonstrate that spatial structure can enhance ACE diversity by (i) permitting otherwise mutually exclusive ACs to coexist and (ii) subjecting new AC traits to selection.

doi: 10.1038/s44260-025-00045-z

Gastrulation is an essential process in the early embryonic development of all higher animals. During gastrulation, the three embryonic germ layers, the ectoderm, mesoderm and endoderm, form and move to their correct positions in the developing embryo. This process requires the integration of cell division, differentiation and movement of thousands of cells. These cell behaviours are coordinated through short- and long-range signalling and must involve feedback to execute gastrulation in a reproducible and robust manner. Mechanosensitive signalling pathways and processes are being uncovered, revealing that short- and long-range mechanical stresses integrate cell behaviours at the tissue and organism scale. Because the interactions between cell behaviours, signalling and feedback are complex, combining experimental and modelling approaches is necessary to elucidate the regulatory mechanisms that drive development. We highlight how recent experimental and theoretical studies provided key insights into mechanical feedback that coordinates relevant cell behaviours at the organism scale during gastrulation. We outline advances in modelling the mechanochemical processes controlling primitive streak formation in the early avian embryo and discuss future developments.

doi: 10.1042/BST20240469

Developmental biology has long drawn on dynamical systems to understand the diverging fates and the emerging form of the developing embryo. Cell differentiation and morphogenesis unfold in high-dimensional gene-expression spaces and position spaces. Yet, their stable and reproducible outcomes suggest low-dimensional geometric structures-e.g., fixed points, manifolds, and dynamic attracting and repelling structures-that organize cell trajectories in both spaces. This review surveys the history and recent advances in dynamical systems frameworks for development. We focus on techniques for extracting the organizing geometric structures of cell fate decisions and morphogenetic movements from experiments, as well as their interconnections.

doi: 10.1016/j.semcdb.2025.103620

Embryonic tissues undergo coordinated flows during avian gastrulation to establish the body plan. Here, we elucidate how the interplay between embryonic and extraembryonic tissues affects the chick embryo's size and shape. These two distinct geometric changes are each associated with dynamic curves across which trajectories separate (kinematic repellers). Through physical modeling and experimental manipulations of both embryonic and extraembryonic tissues, we selectively eliminate either or both repellers in model and experiments, revealing their mechanistic origins. We find that embryo size is affected by the competition between extraembryonic epiboly and embryonic myosin-driven contraction-which persists when mesoderm induction is blocked. Instead, the characteristic shape change from circular to pear-shaped arises from myosin-driven cell intercalations in the mesendoderm, irrespective of epiboly. These findings elucidate modular mechanisms controlling avian gastrulation flows and provide a mechanistic basis for the independent control of embryo size and shape during development.

doi: 10.1038/s41467-025-60249-8

During vertebrate gastrulation, an embryo transforms from a layer of epithelial cells into a multilayered gastrula. This process requires the coordinated movements of hundreds to tens of thousands of cells, depending on the organism. In the chick embryo, patterns of actomyosin cables spanning several cells drive coordinated tissue flows. Here, we derive a minimal theoretical framework that couples actomyosin activity to global tissue flows. Our model predicts the onset and development of gastrulation flows in normal and experimentally perturbed chick embryos, mimicking different gastrulation modes as an active stress instability. Varying initial conditions and a parameter associated with active cell ingression, our model recapitulates distinct vertebrate gastrulation morphologies, consistent with recently published experiments in the chick embryo. Altogether, our results show how changes in the patterning of critical cell behaviors associated with different force-generating mechanisms contribute to distinct vertebrate gastrulation modes via a self-organizing mechanochemical process.

doi: 10.1126/sciadv.adh8152

Prior research on evolutionary mechanisms during the origin of life has mainly assumed the existence of populations of discrete entities with information encoded in genetic polymers. Recent theoretical advances in autocatalytic chemical ecology establish a broader evolutionary framework that allows for adaptive complexification prior to the emergence of bounded individuals or genetic encoding. This framework establishes the formal equivalence of cells, ecosystems and certain localized chemical reaction systems as autocatalytic chemical ecosystems (ACEs): food-driven (open) systems that can grow due to the action of autocatalytic cycles (ACs). When ACEs are organized in meta-ecosystems, whether they be populations of cells or sets of chemically similar environmental patches, evolution, defined as change in AC frequency over time, can occur. In cases where ACs are enriched because they enhance ACE persistence or dispersal ability, evolution is adaptive and can build complexity. In particular, adaptive evolution can explain the emergence of self-bounded units (e.g. protocells) and genetic inheritance mechanisms. We do this by laying out the parallels between a living cell (or organism) and a local ecosystem and between a population of cells/organisms and a meta-ecosystem of interconnected local ecosystems. This implies that both ecological change (e.g. ecological succession) and Darwinian evolution can be seen as formally equivalent in that each entails changes in the frequency of ACs in a meta-ecosystem. We then tie this insight to the origin of life and explore the two main differences between ecological change and Darwinian evolution, namely compartmentalization and genetics, and describe how prebiotic chemical processes might have bridged this apparent gap by gradually becoming more evolution-like and less ecology-like over time. We end by proposing that the conception of cells as chemical ecosystems provides a powerful new framework for guiding both theoretical and empirical studies of the origins of life.

doi: 10.1098/rsif.2023.0346

It is becoming widely accepted that very early in life's origin, even before the emergence of genetic encoding, reaction networks of diverse small chemicals might have manifested key properties of life, namely self-propagation and adaptive evolution. To explore this possibility, we formalize the dynamics of chemical reaction networks within the framework of chemical ecosystem ecology. To capture the idea that life-like chemical systems are maintained out of equilibrium by fluxes of energy-rich food chemicals, we model chemical ecosystems in well-mixed compartments that are subject to constant dilution by a solution with a fixed concentration of input chemicals. Modelling all chemical reactions as fully reversible, we show that seeding an autocatalytic cycle with tiny amounts of one or more of its member chemicals results in logistic growth of all member chemicals in the cycle. This finding justifies drawing an instructive analogy between an autocatalytic cycle and a biological species. We extend this finding to show that pairs of autocatalytic cycles can exhibit competitive, predator-prey, or mutualistic associations just like biological species. Furthermore, when there is stochasticity in the environment, particularly in the seeding of autocatalytic cycles, chemical ecosystems can show complex dynamics that can resemble evolution. The evolutionary character is especially clear when the network architecture results in ecological precedence, which makes a system's trajectory historically contingent on the order in which cycles are seeded. For all its simplicity, the framework developed here helps explain the onset of adaptive evolution in prebiotic chemical reaction networks, and can shed light on the origin of key biological attributes such as thermodynamic irreversibility and genetic encoding.

doi: 10.1016/j.jtbi.2020.110451