Role of Membrane Fluidity in Pressure Resistance of Escherichia coli NCTC 8164

Abstract

The relationship among growth temperature, membrane fatty acid composition, and pressure resistance was examined in Escherichia coli NCTC 8164. The pressure resistance of exponential-phase cells was maximal in cells grown at 10°C and decreased with increasing growth temperatures up to 45°C. By contrast, the pressure resistance of stationary-phase cells was lowest in cells grown at 10°C and increased with increasing growth temperature, reaching a maximum at 30 to 37°C before decreasing at 45°C. The proportion of unsaturated fatty acids in the membrane lipids decreased with increasing growth temperature in both exponential- and stationary-phase cells and correlated closely with the melting point of the phospholipids extracted from whole cells examined by differential scanning calorimetry. Therefore, in exponential-phase cells, pressure resistance increased with greater membrane fluidity, whereas in stationary-phase cells, there was apparently no simple relationship between membrane fluidity and pressure resistance. When exponential-phase or stationary-phase cells were pressure treated at different temperatures, resistance in both cell types increased with increasing temperatures of pressurization (between 10 and 30°C). Based on the above observations, we propose that membrane fluidity affects the pressure resistance of exponential- and stationary-phase cells in a similar way, but it is the dominant factor in exponential-phase cells whereas in stationary-phase cells, its effects are superimposed on a separate but larger effect of the physiological stationary-phase response that is itself temperature dependent

Phospholipids modify substrate binding and enzyme activity of human cytochrome P450 27A1

“…Being strain specific, lipid profiles of E. coli membranes nevertheless overlap (22,44,45). Ions corresponding to the m/z of several of these fatty acids were seen in the mass spectra of P450 lipid extracts (Figs.…”

Solutes determine the temperature windows for microbial survival and growth

“…(ii) Sucrose and NaCl (both kosmotropic) protect Lactococcus lactis against potentially lethal high-pressure treatments (28). (iii) Low temperatures enhance pressure tolerance of stationary phase E. coli cells (29). (iv) Enzyme and membrane assays show metabolic activities enhanced by glycerol at low temperature (10), and (v) studies show ethanol-induced cold tolerance of yeasts and bacteria (11,24).…”

Induction of Oxidative Stress by High Hydrostatic Pressure in Escherichia coli

“…Both protein denaturation and membrane disruption have been amply demonstrated in bacterial cells treated with HHP and shown to result in inactivation of key enzymes and processes (18,39,43) and functional and structural disruption of cellular structures and membranes (19,35,37,46). Currently, the accumulation of protein and membrane damage is believed to be at the basis of bacterial inactivation by HHP, and both chaperones and membrane fluidity have recently been linked with increased pressure resistance (2,13). However, whether these types of damage are the direct and only cause of cell death remains uncertain.…”