Fatty acid profile of Escherichia coli during the heat‐shock response

Abstract

The possible changes in the fatty acid profile of Escherichia coli during heat‐shock have been investigated. Bacteria growing in steady‐state at 30°C were subjected to an abrupt temperature upshift to 45°C and held at the high temperature for various periods of time in order to elicit the heat‐shock response. Fatty acid compositions of lipids extracted from samples taken at different times after the temperature upshift, as well as from cultures in steady‐state at 30 and 45°C, were determined by gas‐chromatography. It has been found that the total unsaturates to total saturates ratio decreases gradually during heat‐shock and that 30 min after the temperature jump, the reduction is equivalent to 57% of the difference between ratios corresponding to steady‐state cultures at 30 and 45°C. Consistent with this remodeling of lipid acyl chains, there is a decrease in the excimerization rate of the fluidity probe dipyrenylpropane incorporated into sonicated E. coli lipid extracts. Such modifications occur within the time‐span of the heat‐shock response, as judged from our previous measurements of the kinetics of change in heat‐shock proteins induction ratio. Together, these results indicate that the control of membrane fluidity during the heat‐shock response can be accounted for, at least in part, by an important change in the fatty acid composition of Escherichia coli lipids.

Treatment ofSalmonella entericaSerovar Enteritidis with a Sublethal Concentration of Trisodium Phosphate or Alkaline pH Induces Thermotolerance

“…Growth conditions such as the composition of the growth medium (2,3,35,60), the growth phase (age) of the cells (35,42,50,75), the incubation temperature at which the bacteria were cultured (2,35,55,56,60,70), and the pH (10,56,60) markedly affect the composition of the membrane lipid. E. coli cells subjected to an abrupt temperature shift from 30 to 45°C and held at the high temperature for various periods of time revealed a gradual decrease in the total unsaturated to saturated fatty acid ratio in the cytoplasmic membrane, resulting in reduced membrane fluidity and a higher melting point (43). This reduction in membrane fluidity correlated with the cellular heat shock response, as detected by the change in the induction levels of GroEL and DnaK (40,43).…”

“…E. coli cells subjected to an abrupt temperature shift from 30 to 45°C and held at the high temperature for various periods of time revealed a gradual decrease in the total unsaturated to saturated fatty acid ratio in the cytoplasmic membrane, resulting in reduced membrane fluidity and a higher melting point (43). This reduction in membrane fluidity correlated with the cellular heat shock response, as detected by the change in the induction levels of GroEL and DnaK (40,43). In Pediococcus sp.…”

Synechocystis HSP17 is an amphitropic protein that stabilizes heat-stressed membranes and binds denatured proteins for subsequent chaperone-mediated refolding

“…5C). By assuming that even the high melting lipid components of membranes adapt a fluid or ''hyperfluid'' state during heat stress (19,20,28), the apparent lipid phase state specificity of the HSP17-lipid interaction highlights a potentially important physiological role in membrane thermostabilization.…”

Human IAPP amyloidogenic properties and pancreatic β-cell death

“…To survive, all living organisms depend on stress responses of which, the most evolutionarily conserved, is the heat-shock response (HSR) [99,100]. Discovered in Drosophila, it is a cellular response present in all organisms including prokaryotes [101,102]. Model systems are very important to study stress.…”