In Escherichia coli, the growth rate at elevated temperatures is controlled by the availability of endogenous methionine, which is limited because of the temperature sensitivity of the metA gene product, homoserine transsuccinylase (HTS). In order to determine the relationship between this control mechanism and the heat shock response, we estimated the cellular levels of HTS during heat shock by Western (immunoblot) analysis and found an increase following induction by temperature shift and by addition of ethanol or cadmium ions. The elevated level of HTS was a result of transcriptional activation of the metA gene. This activation was heat shock dependent, as it did not take place in rpoH mutants, and probably specific to the metA gene, as another gene of the methionine regulon (metE) was not activated. These results suggest a metabolic link between the two systems that control the response of E. coli to elevated temperatures: the metA gene, which codes for the enzyme responsible for regulating cell growth as a function of temperature elevation (HTS), is transcriptionally activated by the heat shock response.