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Biology subjects

Oswald, T. A.

Publications and source records attributed to Oswald, T. A..

3 recordsLinked to original sources

Mechanical Implications of Cellular Viscoelasticity, Cortex Polarity, Superelasticity, and Cell-Cell Junctions in Curved Tissues

Investigations of the response of curved epithelia derived from MDCK-II cells to external deformation involved indentation-relaxation experiments using colloidal probe microscopy. Notably, hemicysts exhibited lower tissue tension, greater compliance, and increased fluidity compared to cysts. The primary response to deformation turned out to be the in-plane expansion of the basal cortex/membrane of cells. Additionally, drug treatments applied to curved tissue, along with deformation of tailored mutants (such as E-cadherin knockout), revealed that tissue compliance over short time scales is influenced by an interplay of viscoelastic properties in individual cells, their apical-basal polarity, superelasticity of the shell, and excess interfacial area. Meanwhile, tissue resilience predominantly depends on the integrity of cell-cell contacts.

biophysics↗

Active fluctuations of cells reduce friction to enable fast and coherent collective migration

Collective cell migration is an emergent phenomenon, with long-range cell-cell communication influenced by various factors, including transmission of forces, viscoelasticity of individual cells, substrate interactions, and mechanotransduction. We investigate how alterations in cell-substrate distance fluctuations, cell-substrate adhesion, and traction forces impact the average velocity and temporal-spatial correlation of confluent monolayers formed either by wild-type MDCKII cells or zonula occludens (ZO) 1/2-depleted MDCKII cells (dKD) representing highly contractile cells. The data indicates that confluent dKD monolayers exhibit decreased average velocity compared to less contractile WT cells concomitant with increased substrate adhesion, reduced traction forces, a more compact shape, diminished cell-cell interactions, and reduced cell-substrate distance fluctuations. Depletion of basal actin and myosin further supports the notion that short-range cell-substrate interactions, particularly fluctuations driven by basal actomyosin, significantly influence the migration speed of the monolayer on a larger length scale.

biophysics↗

Tight junction ZO proteins maintain tissue fluidity, ensuring efficient collective cell migration

Tight junctions are essential components of epithelial tissues connecting neighboring cells to provide protective barriers. Albeit their general function to seal compartments is well understood, their role in collective cell migration is largely unexplored. Here, the importance of the tight junction proteins ZO1 and ZO2 for epithelial migration is investigated employing video microscopy in conjunction with velocimetry, segmentation, cell tracking, and atomic force microscopy/spectroscopy. The results indicate that ZO proteins are necessary for fast and coherent migration. In particular, ZO1 and 2 loss (dKD) induces actomyosin remodeling away from the central cortex towards the periphery of individual cells, resulting in altered viscoelastic properties. A tug-of-war emerges between two subpopulations of cells with distinct morphological and mechanical properties: 1) smaller and highly contractile cells with an outward-bulged apical membrane, and 2) larger, flattened cells, which, due to tensile stress, display a higher proliferation rate. In response, the cell density increases, leading to crowding-induced jamming and more small cells over time. Co-cultures comprising wildtype and dKD cells display phase separation based on differences in contractility rather than differential adhesion. This study shows that ZO proteins are necessary for efficient collective cell migration by maintaining tissue fluidity and controlling proliferation.

biophysics↗