Biophysical Society Thematic Meeting | Riga 2026

Active and Responsive Soft Matter: From Biological to Engineered Systems

Poster Abstracts

15-POS Board 15 LOCAL FORCES IN THE BACTERIAL CELL ENVELOPE AND THE MECHANISM OF OSMOADAPTATION Andriy Anishkin 1 ; Elissa Moller 1 ; Sergei Sukharev 1 ; 1 University of Maryland, Biology and IPST, College Park, MD, USA Freshwater is the primary transmission route for enteric pathogens and commensals, requiring robust adaptation to external osmolarity drops. To endure environmental shifts, bacteria rapidly eject small metabolites via tension-activated channels, MscS and MscL, residing in the inner membrane in high numbers (~10^3 per cell). For a few milliseconds, the permeability of the cytoplasmic membrane may increase by 10 orders of magnitude. How does this response, mediated by a population of low-tension-activated channels (MscS), align with a non-leaky cytoplasmic membrane and proton-based bacterial energetics? We propose that the activity of the MscS population is tightly regulated. During steady growth, most channels stay in a tension-insensitive inactivated state but can be reactivated during osmotic shock to release osmolytes. (1) We have shown that the commonly observed splayed conformation of MscS is the inactivated state, stabilized by lipids separating the peripheral helices that form the gate. (2) Our simulations predict that the tension-receiving helices can be reconnected to the gate by applying turgor pressure, which pushes the gate toward the periplasm, expels lipids, and compacts the structure. (3) Light-scattering traces from rapid-dilution experiments on bacterial suspensions indicated that cells swell significantly before tension reaches the channel activation threshold, indicating an excess of inner-membrane area. Under the shock, turgor rises to 8-12 atm, thereby re-sensitizing the inactivated MscS population before tension reaches the activation threshold. (4) After solute release, the total cell volume decreases, increasing cytoplasmic macromolecular crowding that immediately inactivates MscS and terminates the permeability response. Therefore, the adaptive cycle of MscS tracks the sequential changes in local mechanical stress: a surge in turgor recharges the channels and prepares them to open under tension. As a result, the entire MscS population can remain in a tension-insensitive state until osmotic shock occurs.

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