Biology subjects

Vermeil, J.

Publications and source records attributed to Vermeil, J..

5 recordsLinked to original sources

bioRxiv2026

Softer when Thicker: a Conserved Scaling Law Governs Actin Cortex Mechanics

Scaling laws are powerful tools in material science to relate geometric and mechanical properties of materials. The actin cortex, a dynamic network beneath the plasma membrane, is essential for cellular morphogenesis, force generation, and tissue organization. Despite its critical role, the mechanical properties of the cortex itself remain poorly understood. Using the magnetic pincher, a new technique we recently developed, we directly measure the thickness (h) and elastic modulus (E) of the actin cortex in live cells, uncovering a universal scaling (E ~ h-2) across multiple cell types. Drawing an analogy to cellular solids, common in nature and material science, we identified an origin for this scaling: the volume fraction of actin filaments varies concomitantly with the cortex thickness, due to a conservation of filamentous actin quantity. Thus thinner cortices exhibit higher actin density and stiffness, while thicker cortices are sparser and softer. The relationship holds under diverse perturbations targeting myosin contractility, actin nucleation, and turnover, but is lost upon actin disassembly, highlighting its dependence on the intact actin network. Our results establish that cells, across cell types, function within a rather limited range of quantity of cortical actin filaments and primarily modulate cortex thickness to tune mechanical properties, with profound implications for cell shape regulation, tissue mechanics, and the interpretation of indentation-based mechanical measurements.

biophysics↗

bioRxiv2025

Allometric spreading and focal adhesion collective organization are coordinated by cell-scale geometrical constraints

Focal adhesions are protein complexes that transmit actin cytoskeleton forces to the extracellular matrix and serve as signaling hubs that regulate cell physiology. While their growth is achieved through a local force-dependent process, the requirement of sustaining stress at the cell scale suggests a global regulation of the collective organization of focal adhesions. To investigate evidence of such large-scale regulation, we compared changes in cell shape and the organization of focal adhesion-like structures during the early spreading of fibroblasts either on a two-dimensional substrate or confined between two parallel plates, and for cells of different volumes. In this way, we reveal that the areal density of focal adhesions is conserved regardless of cell size or third-dimensional confinement, despite different absolute values of the surface covered by adhesion clusters. In particular, the width of the focal adhesions ring, which fills the flat lamella at the cell front, adapts to cell size and third-dimensional confinement and scales with cell-substrate contact radius. We find that this contact radius also adapts in the parallel-plate geometry so that the cumulated area of cellsubstrate contact is conserved at the cell scale. We suggest that this behavior is the result of 3D cell shape changes which govern spreading transitions. Indeed, because of volume conservation constraints, the evolution of cell-body contact angle adjusts according to cell size and confinement, whereas the rate of early spreading at the cell-substrate contact is not affected by thirddimensional geometry. Overall, our data suggest that a coordination between global and local scales mediates the adaptation of cell-substrate contacts and focal adhesions distribution to large scale geometrical constraints, which allows an invariant cell-substrate adhesive energy.

biophysics↗

bioRxiv2023

The membrane-actin linkers ezrin, radixin, and moesin are dispensable for macrophage migration and cortex mechanics.

The cellular actin cortex provides crucial mechanical support and plays critical roles in numerous functions, including cell division and migration. The proteins of the ERM family, ezrin, radixin, and moesin, are central to these processes by linking the plasma membrane to the actin cytoskeleton. To investigate the individual contributions of these three proteins to leukocyte migration, we generated single and triple ERM knock-out macrophages. Surprisingly, we found that even in the absence of ERMs, macrophages can still form the different actin structures promoting cell migration, such as filopodia, lamellipodia, podosomes, and ruffles. Furthermore we discovered that, unlike every other cell type previously investigated, the single or triple knock-out of ERMs does not affect macrophage migration in a large diversity of contexts. Finally, we demonstrated that the loss of ERMs in macrophages does not affect the mechanics of their actin cortex. These findings challenge the notion that ERMs are universally essential for cortex mechanics and cell migration and support the notion that the macrophage cortex may have diverged from that of other cells to allow for their adaptive cortical plasticity.

cell biology↗

bioRxiv2023

The distance between the plasma membrane and the actomyosin cortex acts as a nanogate to control cell surface mechanics

Animal cell shape changes are controlled by the actomyosin cortex, a peripheral actin network tethered to the plasma membrane by membrane-to-cortex attachment (MCA) proteins. Previous studies have focused on how myosin motors or actin turnover can generate the local deformations required for morphogenesis. However, how the cell controls local actin nucleation remains poorly understood. By combining molecular engineering with biophysical approaches and in situ characterization of cortical actin network architecture, we show that membrane-to-cortex tethering determines the distance between the plasma membrane and the actomyosin cortex at the nanoscale of single actin nucleators. In turn, the size of this gap dictates actin filament production and the mechanical properties of the cell surface. Specifically, it tunes formin activity, controlling actin bundling and cortical tension. Our study defines the membrane-to-cortex distance as a nanogate that cells can open or close by MCA proteins to control the activity of key molecules at the cell surface.

biophysics↗

bioRxiv2022

Mechanoregulation of biofilm architecture promotes Pseudomonas aeruginosa antibiotic tolerance.

In the wild, bacteria are most frequently found in the form of multicellular structures called biofilms1. Biofilms grow at the surface of abiotic and living materials with wide-ranging mechanical properties. Despite their co-occurrence during infection, we still lack a clear understanding of how mechanics regulate biofilm architecture and the physiology of resident bacteria. The opportunistic pathogen Pseudomonas aeruginosa forms biofilms on indwelling medical device2 and on soft tissues including burn wounds and the airway mucosa3. Here, we demonstrate that mechanical properties of hydrogel material substrates define P. aeruginosa biofilm architecture. We show that hydrogel mesh size regulates twitching motility, a surface exploration mechanism priming biofilms, ultimately controlling the arrangement of single cells in the multicellular community. The resulting architectural transitions increase P. aeruginosas tolerance to colistin, a last resort antibiotic. Our results thereby establish material properties as a regulator of biofilm architecture and antibiotic efficacy.

microbiology↗