Speaker
Description
Tissue morphogenesis emerges from the collective mechanical behaviour of epithelial cells, where gene expression, cytoskeletal dynamics and cell cycle progression combine to drive coordinated tissue-scale deformations. Neural tube closure is a paradigmatic example whose failure gives rise to severe congenital conditions including spina bifida. Yet quantitative links between gene-level perturbations, single-cell mechanics and tissue-scale closure outcomes remain missing. Here we develop a data-driven vertex model that bridges these scales, parameterised directly from quantitative imaging across developmental stages. Incorporating cell cycle dynamics and apical constriction as mechanistically grounded inputs, the model recapitulates tissue-scale deformation during closure and correctly predicts neuropore widening under pharmacological inhibition of contractility.
This provides a framework in which genetic perturbations altering cytoskeletal tension or cell cycle progression can be mapped directly onto closure outcomes offering a quantitative route to understanding how mutations disrupting neuroepithelial mechanics lead to neural tube defects.
