Dynamic morphoskeletons

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

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