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Biology subjects

Vermeil, J.

Publications and source records attributed to Vermeil, J..

3 recordsLinked to original sources

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↗

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↗

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↗