For most cells, a sudden decrease in external osmolarity results in fast water influx that can burst the cell. To survive, cells rely on the passive response of mechanosensitive channels, which open under increased membrane tension and allow the release of cytoplasmic solutes and water. Although the gating and the molecular structure of mechanosensitive channels found in Escherichia coli have been extensively studied, the overall dynamics of the whole cellular response remain poorly understood. Here, we characterize E. coli's passive response to a sudden hypoosmotic shock (downshock) on a single-cell level. We show that initial fast volume expansion is followed by a slow volume recovery that can end below the initial value. Similar response patterns were observed at downshocks of a wide range of magnitudes. Although wild-type cells adapted to osmotic downshocks and resumed growing, cells of a double-mutant (ΔmscL, ΔmscS) strain expanded, but failed to fully recover, often lysing or not resuming growth at high osmotic downshocks. We propose a theoretical model to explain our observations by simulating mechanosensitive channels opening, and subsequent solute efflux and water flux. The model illustrates how solute efflux, driven by mechanical pressure and solute chemical potential, competes with water influx to reduce cellular osmotic pressure and allow volume recovery. Our work highlights the vital role of mechanosensation in bacterial survival.osmotic downshock | bacterial mechanosensing | single-cell imaging B iology offers an array of intriguing mechanical solutions, both active and passive, often exceeding what is currently possible with man-made methods. Understanding how biological systems achieve different functionalities under mechanical stimuli can inform new, thus-far-unexplored design principles. One such passive control system is the bacterial response to sudden decreases in external osmolarities.A Gram-negative cell's fluid cytoplasm is separated from the external environment by the inner membrane, the periplasmic space, and the outer membrane. Ordinarily, the total solute concentration within the cytoplasm is higher than that of the environment, resulting in a positive osmotic pressure on the cell wall (termed turgor pressure) (1). Escherichia coli is able to respond to both increases and decreases in external concentrations. An increase in external osmolarity (hyperosmotic shock or upshock) results in water efflux from the cell interior, causing cellular volume to shrink and osmotic pressure to drop to zero (2). E. coli responds by actively accumulating specific solutes (osmolytes), such as potassium, proline, and glycine-betaine (2). Accumulation of osmolytes in the cell's cytoplasm causes reentry of water, cell volume increase, and recovery of osmotic pressure (3, 4). A downward shift in external osmolarity (termed hypoosmotic shock or downshock) causes fast water influx into the cell's cytoplasm. As a result, the osmotic pressure increases and the cell expands in a nonlinear fashion (5,6