Current & Upcoming

Embryogenesis integrates morphogenesis—coordinated cell movements—with cell differentiation. 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 can mediate 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.

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. 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.

TBA