2021
Pablo A. Fernández; Benedikt Buchmann; Andriy Goychuk; Lisa K. Engelbrecht; Marion K. Raich; Christina H. Scheel; Erwin Frey; Andreas R. Bausch
Surface-tension-induced budding drives alveologenesis in human mammary gland organoids Journal Article
In: Nature Physics, vol. 17, no. 10, pp. 1130–1136, 2021, ISSN: 1745-2473, 1745-2481.
Abstract | Links | BibTeX | Tags: Analytical Theory, Budding, Cell Migration, Collective Dynamics, Morphogenesis, Organoids, Shape Instability
@article{fernandez_surface-tension-induced_2021,
title = {Surface-tension-induced budding drives alveologenesis in human mammary gland organoids},
author = {Pablo A. Fernández and Benedikt Buchmann and Andriy Goychuk and Lisa K. Engelbrecht and Marion K. Raich and Christina H. Scheel and Erwin Frey and Andreas R. Bausch},
url = {https://www.nature.com/articles/s41567-021-01336-7},
doi = {10.1038/s41567-021-01336-7},
issn = {1745-2473, 1745-2481},
year = {2021},
date = {2021-10-01},
urldate = {2026-05-29},
journal = {Nature Physics},
volume = {17},
number = {10},
pages = {1130–1136},
abstract = {Organ development involves complex shape transformations driven by active mechanical stresses that sculpt the growing tissue1,2. Epithelial gland morphogenesis is a prominent example where cylindrical branches transform into spherical alveoli during growth3,4,5. Here we show that this shape transformation is induced by a local change from anisotropic to isotropic tension within the epithelial cell layer of developing human mammary gland organoids. By combining laser ablation with optical force inference and theoretical analysis, we demonstrate that circumferential tension increases at the expense of axial tension through a reorientation of cells that correlates with the onset of persistent collective rotation around the branch axis. This enables the tissue to locally control the onset of a generalized Rayleigh–Plateau instability, leading to spherical tissue buds6. The interplay between cell motion, cell orientation and tissue tension is a generic principle that may turn out to drive shape transformations in other cell tissues.},
keywords = {Analytical Theory, Budding, Cell Migration, Collective Dynamics, Morphogenesis, Organoids, Shape Instability},
pubstate = {published},
tppubtype = {article}
}
Felix Kempf; Andriy Goychuk; Erwin Frey
Tissue flow through pores: a computational study Miscellaneous
2021.
Abstract | Links | BibTeX | Tags: Cell Migration, Cell Polarization, Cellular Potts Model, Collective Dynamics, Confined Migration, Simulation
@misc{kempf_tissue_2021,
title = {Tissue flow through pores: a computational study},
author = {Felix Kempf and Andriy Goychuk and Erwin Frey},
url = {http://biorxiv.org/lookup/doi/10.1101/2021.03.25.436985},
doi = {10.1101/2021.03.25.436985},
year = {2021},
date = {2021-03-01},
urldate = {2026-05-29},
publisher = {Biophysics},
abstract = {Cell migration is of major importance for the understanding of phenomena such as morphogenesis, cancer metastasis, or wound healing. In many of these situations cells are under external confinement. In this work we show by means of computer simulations with a Cellular Potts Model (CPM) that the presence of a bottleneck in an otherwise straight channel has a major influence on the internal organisation of an invading cellular monolayer and the motion of individual cells therein. Comparable to a glass or viscoelastic material, the cell sheet is found to exhibit features of both classical solids and classical fluids. The local ordering on average corresponds to a regular hexagonal lattice, while the relative motion of cells is unbounded. Compared to an unconstricted channel, we observe that a bottleneck perturbs the formation of regular hexagonal arrangements in the epithelial sheet and leads to pile-ups and backflow of cells near the entrance to the constriction, which also affects the overall invasion speed. The scale of these various phenomena depends on the dimensions of the different channel parts, as well as the shape of the funnel domain that connects wider to narrower regions.},
keywords = {Cell Migration, Cell Polarization, Cellular Potts Model, Collective Dynamics, Confined Migration, Simulation},
pubstate = {published},
tppubtype = {misc}
}
2019
Florian Thüroff; Andriy Goychuk; Matthias Reiter; Erwin Frey
Bridging the gap between single-cell migration and collective dynamics Journal Article
In: eLife, vol. 8, pp. e46842, 2019, ISSN: 2050-084X.
Abstract | Links | BibTeX | Tags: Cell Migration, Cell Polarization, Cellular Potts Model, Collective Dynamics, Simulation, Wound Healing
@article{thuroff_bridging_2019,
title = {Bridging the gap between single-cell migration and collective dynamics},
author = {Florian Thüroff and Andriy Goychuk and Matthias Reiter and Erwin Frey},
url = {https://elifesciences.org/articles/46842},
doi = {10.7554/eLife.46842},
issn = {2050-084X},
year = {2019},
date = {2019-12-01},
urldate = {2026-05-29},
journal = {eLife},
volume = {8},
pages = {e46842},
abstract = {Motivated by the wealth of experimental data recently available, we present a cellular-automaton-based modeling framework focussing on high-level cell functions and their concerted effect on cellular migration patterns. Specifically, we formulate a coarse-grained description of cell polarity through self-regulated actin organization and its response to mechanical cues. Furthermore, we address the impact of cell adhesion on collective migration in cell cohorts. The model faithfully reproduces typical cell shapes and movements down to the level of single cells, yet allows for the efficient simulation of confluent tissues. In confined circular geometries, we find that specific properties of individual cells (polarizability; contractility) influence the emerging collective motion of small cell cohorts. Finally, we study the properties of expanding cellular monolayers (front morphology; stress and velocity distributions) at the level of extended tissues.},
keywords = {Cell Migration, Cell Polarization, Cellular Potts Model, Collective Dynamics, Simulation, Wound Healing},
pubstate = {published},
tppubtype = {article}
}