Summary: The stress-sensing systems leading to the cellular heat shock response (HSR) and the mechanism responsible for the desensitizing of this response in stress-acclimated cells are largely unknown. Here it is demonstrated that there is a close correlation between a 3 ° increase in the temperature required for maximal activation of a heat-shock (HS)-inducible gene in and an increase in the percentage of cellular unsaturated fatty acids when cells are subjected to extended periods of growth at 37 °. The latter occurs with the same kinetics as HS gene down-regulation during a prolonged HS and is reversed by reacclimation to growth at 25 °. The transient nature of the HS may therefore be due to a lipid-mediated decrease in cellular heat sensitivity. Further evidence that unsaturated fatty acids desensitize cells to heat, with a resultant down-regulation of the HSR, is provided by demonstrating a 9 ° increase in the temperature required for maximal induction of this HS-inducible gene in cells containing high levels of unsaturated fatty acids assimilated during anaerobic growth at 25 °.


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