Professor University of Notre Dame Notre Dame, Indiana, United States
Introduction: : Understanding the biochemical and mechanical cues that cause epithelial sheets to reorganize themselves into three-dimensional organs remains a central challenge in biology. During Drosophila wing-disc eversion, a pseudostratified pouch folds outward and fuses into a bilayer that goes on to form the adult wing. This project unites quantitative experiments with a 3D multiscale mechano-chemical (M3D) model to decode the late-stage morphogenesis of the Drosophila wing imaginal disc during eversion. The work couples: (i) a GPU-accelerated particle-based model that resolves apical, basal and extracellular-matrix mechanics on a deforming epithelial surface; (ii) reaction–diffusion models for hormone (ecdysone) and morphogen signaling (Dpp, Wg) extended down to intracellular Rho1/Cdc42 dynamics; and (iii) machine-learning pipelines—Gaussian-process surrogate modeling, Bayesian optimization and neural-network solvers—to calibrate and accelerate simulations against time-lapse light-sheet imaging, biomechanical perturbations and quantitative immunostaining. Iterative experimentation will map how spatially patterned actomyosin contractility, cell-ECM adhesion and ECM stiffness drive coordinated cell reshaping, layer coupling and tissue folding. The resulting framework will yield predictive, systems-level insights into how hormonal timing interfaces with morphogen gradients to orchestrate organ-scale shape changes.
Materials and
Methods: : Using a physics based coarse-grained 3D model to capture dynamics of fold formation during Drosophila wing disc eversion. The wing disc goes through a drastic shape change at this stage in development without significant cell proliferation. We use strain tensors and poisson ratios to emulate T1 rearrangements in the tissue causing the fold formation. We also investigate the role of MyoVI in these rearrangements and tissue shape change.
Results, Conclusions, and Discussions:: MyoVI knockdown causes the final organ shape to be morphed and the fold formation to not be as drastic as in wild type eversion. The strain tensor applied on our coarse grained mesh causes the desired shape change. Coupling this with chemical signaling offers more insight into it as detailed in my abstract.
