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Tabler, J.

Publications and source records attributed to Tabler, J..

2 recordsLinked to original sources

Multifractal signatures in ossification reveal a disordered-to-ordered transition in mineral pattern

Developing biological systems can exhibit both dynamic pattern formation and cross-scale interactions. Multiscale relationships are critical in the establishment of these patterns but remain poorly understood. Classification of mineral pattern in bone is a quintessential example. One approach to quantifying these patterns relies upon statistical self-similarity and, in particular, monofractal analysis. However, simple monofractal characterisations fail to capture the complexity of multiscale interactions in developing biological systems. Here we show that multifractal techniques, effectively capture the complex patterns of self-similarity in a dimensionally reduced, usable way. Further, we show that a simple generative model of ossification in the mouse skull, coupled with multifractal methods indicates a primary role of collagen density in pattern establishment and predicts the existence of a sharp boundary in pattern complexity.

biophysics↗

Self-propagating wave drives noncanonical antidurotaxis of skull bones in vivo

Cell motility is a key feature of tissue morphogenesis, and it is thought to be driven primarily by the active migration of individual cells or collectives. However, this model is unlikely to apply to cells lacking overt cytoskeletal, stable cell-cell or cell-cell adhesions, and molecular polarity, such as mesenchymal cells. Here, by combining a novel imaging pipeline with biophysical modeling, we discover that during skull morphogenesis, a self-generated collagen gradient expands a population of osteoblasts towards a softer matrix. Biomechanical measurements revealed a gradient of stiffness and collagen along which cells move and divide. The moving cells generate an osteogenic front that travels faster than individual tracked cells, indicating that expansion is also driven by cell differentiation. Through biophysical modeling and perturbation experiments, we found that mechanical feedback between stiffness and cell fate drives bone expansion and controls bone size. Our work provides a mechanism for coordinated motion that does not rely upon the cytoskeletal dynamics of cell migration. We term this self-propagating motion down a stiffness gradient, noncanonical antidurotaxis. Identification of alternative mechanisms of cellular motion will help in understanding how directed cellular motility arises in complex environments with inhomogeneous material properties.

biophysics↗