Pere Roca‐Cusachs

The paper identifies how amphipathic helices bind to the inner nuclear membrane by sensing lipid packing defects rather than electrostatics, showing the INM's loose packing under basal conditions.

The paper shows that keratin bundling in epithelial cells under stretch allows the nucleus to escape its keratin cage, providing a mechanism for tissue adaptation to mechanical stress.

The paper shows extracellular mechanical forces influence Golgi secretory function by modulating carrier biogenesis and exocytosis, with molecular determinants including microtubule acetylation and protein kinase D activity.

The paper shows that fibrillar adhesions control nuclear mechanical response timescales through vimentin cytoskeleton anchoring via plectin 1f.

This paper introduces a strategy to program tissue shape transformations through nematic organization of cellular forces, demonstrating reproducible 3D shape generation upon tissue detachment.

The paper shows Piezo1 senses viscoelasticity in soft ECMs and identifies transcriptomic changes in MSCs in response to matrix properties and Piezo1 activity.

This study shows cells exhibit complex migration patterns along haptotactic gradients, including oscillations and directed movement, and develops a biophysical model to explain these behaviors.

This paper introduces DNA-based hydrogel microparticles with tunable mechanical properties for 3D cellular systems, showing they can be remodeled by fibroblast spheroids based on their stiffness.

The paper investigates the mechanical mechanisms of intestinal cell extrusion, showing that it is driven by calcium-triggered myosin 2A mesh dissolution and lamellipodial forces, with extrusion direction determined by these structures.

This paper introduces 3D-TFM to measure cell-substrate forces in 3D environments and shows cells switch from contractile to extensile behavior as volume decreases.

The paper uses optogenetic Rac1 activation to generate leader cells and shows that collective cell migration requires global mechanical organization rather than autonomous leader action.

The paper shows that nucleocytoplasmic transport (NCT) in cell monolayers responds to mechanical forces but not cell density, contrasting with YAP's response to both mechanics and cell density.

This study shows that cell-matrix forces increase during the loss of naive pluripotency in mESCs and are required for this process.

This study identifies mechanical phenotype differences between LGR5+ and LGR5- colorectal cancer cells, linking them to membrane to cortex attachment proteins and metastatic potential.

The paper shows that competition between biochemical and mechanical cues regulates endothelial cell polarity, driving vascular morphogenesis through tension shifts.