Abstract
Treatment of Escherichia coli with non-lethal doses of heat or benzyl alcohol (BA) causes transient membrane fluidization and permeabilization, and induces the rapid transcription of heat-shock genes in a σ32- dependent manner. This early response is followed by a rapid adaptation (priming) of the cells to otherwise lethal elevated temperature, in strong correlation with an observed remodeling of the composition and alkyl chain unsaturation of membrane lipids. The acquisition of cellular thermotolerance in BA-primed cells is unrelated to protein denaturation and is not accompanied by the formation of major heat-shock proteins, such as GroEL and DnaK. This suggests that the rapid remodeling of membrane composition is sufficient for the short-term bacterial thermotolerance.
Original language | English |
---|---|
Pages (from-to) | 1216-1223 |
Number of pages | 8 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 328 |
Issue number | 4 |
DOIs | |
State | Published - 25 Mar 2005 |
Externally published | Yes |
Keywords
- Acquired thermotolerance
- Heat stress
- Lipid saturation
- Membrane fluidity
- Molecular chaperones
- Thermosensor